subject:(Glutathione Metabolism)

1. NC DOCKS at The University of North Carolina at Greensboro; Shah, Halley. Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism.

Degree: 2013, NC Docks

URL: http://libres.uncg.edu/ir/uncg/f/Shah_uncg_0154M_11276.pdf

► Acrolein is an environmental toxicant, mainly found in smoke released from incomplete combustion of organic matter. The compound is ubiquitously found in endogenous as well… (more)

▼ Acrolein is an environmental toxicant, mainly found in smoke released from incomplete combustion of organic matter. The compound is ubiquitously found in endogenous as well as exogenous environment. Several studies showed that exposure to acrolein can lead to liver damage. The mechanisms involved in acrolein-induced hepatocellular toxicity, however, are not completely understood. This study examines the toxic effects and cytotoxic mechanisms of acrolein on HepG2 cells. Acrolein at pathophysiological concentrations was shown to cause a concentration-dependent decrease in cell viability as measured by MTT and LDH assays. Acrolein exposure was also found to cause apoptotic cell death and an increase in levels of protein carbonyl and TBARS, markers of protein damage and lipid peroxidation, respectively, in HepG2 cells. Acrolein also rapidly depleted intracellular glutathione (GSH), phase II enzyme GSH-linked glutathione-S-transferases (GST) and aldose reductase (AR) – three critical cellular defenses that detoxify reactive aldehydes. Results further showed that depletion of cellular GSH by acrolein preceded the loss of cell viability, which suggests that cellular GSH depletion may be an important event in acrolein-induced cytotoxicity. To further determine the role of cellular GSH in protecting against acrolein-mediated cytotoxicity, buthionine sulfoximine (BSO) was used to inhibit cellular GSH biosynthesis. It was observed that depletion of cellular GSH by BSO led to a marked potentiation of acrolein-mediated cytotoxicity in HepG2cells. Furthermore, induction of GSH levels by CDDO-Im, a triterpenoid compound, afforded protection against acrolein toxicity in a concentration-dependent manner. Notably, incubation of HepG2 cells with CDDO-Im at a concentration as low as 10 nM leads to a significant increase in GSH content. To further determine the role of GSH in CDDO-Im-mediated cytoprotection against acrolein-mediated cytotoxicity, BSO was used to inhibit cellular GSH induction by CDDO-Im. Pretreatment of HepG2 cells with BSO and CDDO-Im significantly inhibited CDDO-Im-mediated induction in cellular GSH levels and also reversed cytoprotective effects of CDDO-Im on acrolein-mediated toxicity. In summary, this study demonstrates that exposure to acrolein results in a faster depletion of GSH, an important phase II defense, and causes an increase in apoptosis, lipid peroxidation and protein carbonylation. Furthermore, the endogenous antioxidant GSH can be induced by CDDO-Im. The CDDO-Im-mediated elevated GSH appears to afford a marked protection against acrolein toxicity suggesting that GSH plays a predominant role in CDDO-Im-mediated protection against acrolein-induced toxicity in HepG2 cells. This study may provide understanding on the molecular action of acrolein which may be important to develop novel strategies for the prevention of acrolein-mediated toxicity.

Subjects/Keywords: Acrolein $x Toxicology; Glutathione $x Metabolism

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APA (6^th Edition):

NC DOCKS at The University of North Carolina at Greensboro; Shah, H. (2013). Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism. (Thesis). NC Docks. Retrieved from http://libres.uncg.edu/ir/uncg/f/Shah_uncg_0154M_11276.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

NC DOCKS at The University of North Carolina at Greensboro; Shah, Halley. “Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism.” 2013. Thesis, NC Docks. Accessed January 22, 2021. http://libres.uncg.edu/ir/uncg/f/Shah_uncg_0154M_11276.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

NC DOCKS at The University of North Carolina at Greensboro; Shah, Halley. “Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism.” 2013. Web. 22 Jan 2021.

Vancouver:

NC DOCKS at The University of North Carolina at Greensboro; Shah H. Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism. [Internet] [Thesis]. NC Docks; 2013. [cited 2021 Jan 22]. Available from: http://libres.uncg.edu/ir/uncg/f/Shah_uncg_0154M_11276.pdf.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

NC DOCKS at The University of North Carolina at Greensboro; Shah H. Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism. [Thesis]. NC Docks; 2013. Available from: http://libres.uncg.edu/ir/uncg/f/Shah_uncg_0154M_11276.pdf

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Notre Dame

2. Chen Dai. Novel Metabolic Networks Identify Key Metabolic Hubs of Breast Cancer: The Effect of Aquaporin 7 on Breast Cancer Progression</h1>.

Degree: Chemistry and Biochemistry, 2019, University of Notre Dame

URL: https://curate.nd.edu/show/6108v982n49

► The complex yet interrelated connections between cancer metabolism, gene expression, and oncogenic driver genes have the potential to identify novel biomarkers and drug targets… (more)

▼ The complex yet interrelated connections between cancer metabolism, gene expression, and oncogenic driver genes have the potential to identify novel biomarkers and drug targets with prognostic and therapeutic value. In this thesis, I quantified and compared the levels of 374 metabolites in breast tumor tissue from normal tissue and transgenic mouse breast cancer models overexpressing a panel of oncogenes (PyMT, PyMT-Db, Wnt1, Neu, and C3-TAg). I identified oncogene-specific metabolic profiles and used these model-specific metabolites to predict patient survival. Except for C3-TAg-specific metabolites, the model-specific metabolites were unable to predict survival in breast cancer patients. To further identify the critical metabolic players in breast cancer, we developed a correlation-based network analysis that captures the interactions between metabolic profiling and gene expression data. Our network analysis identified 35 metabolite and 33 gene hubs that had the most network correlations. These hubs have prognostic value and are likely integral to tumor metabolism and breast cancer. I then focused on the gene hub aquaporin-7 (Aqp7), a water and glycerol channel protein, as a novel regulator of breast cancer. AQP7 deficiency in animal models is associated with adipocyte hypertrophy, increased glycerol and triglyceride accumulation, insulin resistance, and obesity. I discovered that AQP7 is a prognostic marker of overall survival and metastasis in breast cancer patients. Aqp7 is expressed in the epithelium and adipocytes in normal and tumor breast tissue. Reduced Aqp7 expression in mouse breast cancer models leads to reduced primary tumor burden and lung metastasis. These data suggest Aqp7 as a target of breast cancer treatment. Further metabolomics and complex lipid profiling of the cells and tumors revealed dramatically altered amino acid, carbohydrate, nucleotide, and lipid metabolism, including lowered glutathione levels and increased lipid levels in Aqp7 knockdown cells and tumors compared to scrambled control. Using cell-based assays, we confirmed that Aqp7 knockdown decreased the oxidative stress tolerance of cancer cells, and altered the usage of arginine. Using an unbiased, discovery-based approach, this study shed light on important players in breast cancer metabolism from a new perspective that complements current guided network analyses. Advisors/Committee Members: Laurie Littlepage, Research Director, Jun Li, Committee Member, Bradley Smith, Committee Member, Anthony Serianni, Committee Member.

Subjects/Keywords: Metabolomics; Lipid Metabolism; Aquaporin 7; Cancer Metabolism; Redox Balance; Glycerol metabolism; Arginine Metabolism; Breast Cancer; Glutathione Metabolism

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APA (6^th Edition):

Dai, C. (2019). Novel Metabolic Networks Identify Key Metabolic Hubs of Breast Cancer: The Effect of Aquaporin 7 on Breast Cancer Progression</h1>. (Thesis). University of Notre Dame. Retrieved from https://curate.nd.edu/show/6108v982n49

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dai, Chen. “Novel Metabolic Networks Identify Key Metabolic Hubs of Breast Cancer: The Effect of Aquaporin 7 on Breast Cancer Progression</h1>.” 2019. Thesis, University of Notre Dame. Accessed January 22, 2021. https://curate.nd.edu/show/6108v982n49.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dai, Chen. “Novel Metabolic Networks Identify Key Metabolic Hubs of Breast Cancer: The Effect of Aquaporin 7 on Breast Cancer Progression</h1>.” 2019. Web. 22 Jan 2021.

Vancouver:

Dai C. Novel Metabolic Networks Identify Key Metabolic Hubs of Breast Cancer: The Effect of Aquaporin 7 on Breast Cancer Progression</h1>. [Internet] [Thesis]. University of Notre Dame; 2019. [cited 2021 Jan 22]. Available from: https://curate.nd.edu/show/6108v982n49.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dai C. Novel Metabolic Networks Identify Key Metabolic Hubs of Breast Cancer: The Effect of Aquaporin 7 on Breast Cancer Progression</h1>. [Thesis]. University of Notre Dame; 2019. Available from: https://curate.nd.edu/show/6108v982n49

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

York University

3. Turnbull, Patrick Carson. Metabolic Manipulation of Glutathione as an Anticancer Therapeutic Target.

Degree: PhD, Kinesiology & Health Science, 2020, York University

URL: https://yorkspace.library.yorku.ca/xmlui/handle/10315/37420

► Many cancers rely on glycolysis rather than mitochondrial metabolism as their primary source of ATP. As such, altering this balance through forced mitochondrial activation has… (more)

▼ Many cancers rely on glycolysis rather than mitochondrial metabolism as their primary source of ATP. As such, altering this balance through forced mitochondrial activation has yielded promising results as anticancer therapies for specific cancers. In previous studies, stimulated mitochondrial activation through exposure to palmitoylcarnitine, a mitochondrial fatty-acid substrate, resulted in colon and prostate cancer-specific cell death, however, mitochondrial fatty-acid oxidation led to increased cervical cancer growth. The primary mechanism for promoting antineoplastic effects in response to palmitoylcarnitine is through oxidative stress, namely through production of superoxide and subsequently hydrogen peroxide (H2O2). However, H2O2 can be hormetic in nature, whereby elevated H2O2 can result in deleterious effects, yet modest H2O2 can promote growth. Therefore, the ability of the cell to regulate H2O2 is of apparent importance, highlighting glutathione, the most abundant intracellular antioxidant, as a potential determinant of cancer survival following palmitoylcarnitine. The purpose of this dissertation was to first determine the response of glutathione to palmitoylcarnitine within relation to cell survival. Following palmitoylcarnitine, glutathione responses seemingly dictated cell fate, whereby HT29 colorectal carcinoma cells displayed decreased cell survival, increased H2O2 and decreased glutathione. CCD 841 normal colon cells were insensitive to palmitoylcarnitine despite increased H2O2, yet maintained glutathione. HepG2 hepatocarcinoma cells, cells associated with fatty-acid stimulated disease progression, increased cell growth with coordinated increases in glutathione following palmitoylcarnitine. This dissertation considered recent evidence that suggests combined inhibition of glutathione and thioredoxin, another intracellular antioxidant, is required for anticancer effects in established tumours. Auranofin is a putative inhibitor of the thioredoxin system. HCT 116 p53-/- cells were resistant to auranofin at doses that HCT 116 p53+/+ cells were sensitive to, however concurrent exposure of auranofin and glutathione depletion through serine and glycine starvation sensitized HCT 116 p53-/- cells to decreased cell survival. This observation was repeated in a p53mutant cell line, HT29. Taken together, this thesis identifies glutathione as an important regulator in determining cell fate in response to palmitoylcarnitine, the dual role of glutathione and thioredoxin in influencing cell fate in relation to p53, and highlights the potential of redox-buffering systems as therapeutic targets for selective antineoplastic growth. Advisors/Committee Members: Perry, Christopher G. R. (advisor).

Subjects/Keywords: Biochemistry; Cancer; Bioenergetics; Mitochondria; Glutathione; Reactive oxygen species (ROS); Thioredoxin; Metabolism

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APA (6^th Edition):

Turnbull, P. C. (2020). Metabolic Manipulation of Glutathione as an Anticancer Therapeutic Target. (Doctoral Dissertation). York University. Retrieved from https://yorkspace.library.yorku.ca/xmlui/handle/10315/37420

Chicago Manual of Style (16^th Edition):

Turnbull, Patrick Carson. “Metabolic Manipulation of Glutathione as an Anticancer Therapeutic Target.” 2020. Doctoral Dissertation, York University. Accessed January 22, 2021. https://yorkspace.library.yorku.ca/xmlui/handle/10315/37420.

MLA Handbook (7^th Edition):

Turnbull, Patrick Carson. “Metabolic Manipulation of Glutathione as an Anticancer Therapeutic Target.” 2020. Web. 22 Jan 2021.

Vancouver:

Turnbull PC. Metabolic Manipulation of Glutathione as an Anticancer Therapeutic Target. [Internet] [Doctoral dissertation]. York University; 2020. [cited 2021 Jan 22]. Available from: https://yorkspace.library.yorku.ca/xmlui/handle/10315/37420.

Council of Science Editors:

Turnbull PC. Metabolic Manipulation of Glutathione as an Anticancer Therapeutic Target. [Doctoral Dissertation]. York University; 2020. Available from: https://yorkspace.library.yorku.ca/xmlui/handle/10315/37420

University of California – San Francisco

4. Anderton, Brittany Nicole. Reprogramming of Glutamate Metabolism and Redox Homeostasis in De Novo MYC-Driven Liver Tumors.

Degree: Biomedical Sciences, 2015, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/3vb4j8p1

► Reprogramming of Glutamate Metabolism and Redox Homeostasis in De Novo MYC-Driven Liver TumorsBrittany AndertonMYC overexpressing cells frequently exhibit increased dependence on uptake of glutamine and… (more)

Subjects/Keywords: Biology; Biochemistry; cancer; glutamine; glutathione; metabolism; miRNAs; MYC

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APA (6^th Edition):

Anderton, B. N. (2015). Reprogramming of Glutamate Metabolism and Redox Homeostasis in De Novo MYC-Driven Liver Tumors. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/3vb4j8p1

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Anderton, Brittany Nicole. “Reprogramming of Glutamate Metabolism and Redox Homeostasis in De Novo MYC-Driven Liver Tumors.” 2015. Thesis, University of California – San Francisco. Accessed January 22, 2021. http://www.escholarship.org/uc/item/3vb4j8p1.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Anderton, Brittany Nicole. “Reprogramming of Glutamate Metabolism and Redox Homeostasis in De Novo MYC-Driven Liver Tumors.” 2015. Web. 22 Jan 2021.

Vancouver:

Anderton BN. Reprogramming of Glutamate Metabolism and Redox Homeostasis in De Novo MYC-Driven Liver Tumors. [Internet] [Thesis]. University of California – San Francisco; 2015. [cited 2021 Jan 22]. Available from: http://www.escholarship.org/uc/item/3vb4j8p1.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Anderton BN. Reprogramming of Glutamate Metabolism and Redox Homeostasis in De Novo MYC-Driven Liver Tumors. [Thesis]. University of California – San Francisco; 2015. Available from: http://www.escholarship.org/uc/item/3vb4j8p1

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

5. Shah, Halley. Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism.

Degree: 2013, University of North Carolina – Greensboro

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=15055

► Acrolein is an environmental toxicant, mainly found in smoke released from incomplete combustion of organic matter. The compound is ubiquitously found in endogenous as well… (more)

▼ Acrolein is an environmental toxicant, mainly found in smoke released from incomplete combustion of organic matter. The compound is ubiquitously found in endogenous as well as exogenous environment. Several studies showed that exposure to acrolein can lead to liver damage. The mechanisms involved in acrolein-induced hepatocellular toxicity, however, are not completely understood. This study examines the toxic effects and cytotoxic mechanisms of acrolein on HepG2 cells. Acrolein at pathophysiological concentrations was shown to cause a concentration-dependent decrease in cell viability as measured by MTT and LDH assays. Acrolein exposure was also found to cause apoptotic cell death and an increase in levels of protein carbonyl and TBARS, markers of protein damage and lipid peroxidation, respectively, in HepG2 cells. Acrolein also rapidly depleted intracellular glutathione (GSH), phase II enzyme GSH-linked glutathione-S-transferases (GST) and aldose reductase (AR) – three critical cellular defenses that detoxify reactive aldehydes. Results further showed that depletion of cellular GSH by acrolein preceded the loss of cell viability, which suggests that cellular GSH depletion may be an important event in acrolein-induced cytotoxicity. To further determine the role of cellular GSH in protecting against acrolein-mediated cytotoxicity, buthionine sulfoximine (BSO) was used to inhibit cellular GSH biosynthesis. It was observed that depletion of cellular GSH by BSO led to a marked potentiation of acrolein-mediated cytotoxicity in HepG2cells. Furthermore, induction of GSH levels by CDDO-Im, a triterpenoid compound, afforded protection against acrolein toxicity in a concentration-dependent manner. Notably, incubation of HepG2 cells with CDDO-Im at a concentration as low as 10 nM leads to a significant increase in GSH content. To further determine the role of GSH in CDDO-Im-mediated cytoprotection against acrolein-mediated cytotoxicity, BSO was used to inhibit cellular GSH induction by CDDO-Im. Pretreatment of HepG2 cells with BSO and CDDO-Im significantly inhibited CDDO-Im-mediated induction in cellular GSH levels and also reversed cytoprotective effects of CDDO-Im on acrolein-mediated toxicity. In summary, this study demonstrates that exposure to acrolein results in a faster depletion of GSH, an important phase II defense, and causes an increase in apoptosis, lipid peroxidation and protein carbonylation. Furthermore, the endogenous antioxidant GSH can be induced by CDDO-Im. The CDDO-Im-mediated elevated GSH appears to afford a marked protection against acrolein toxicity suggesting that GSH plays a predominant role in CDDO-Im-mediated protection against acrolein-induced toxicity in HepG2 cells. This study may provide understanding on the molecular action of acrolein which may be important to develop novel strategies for the prevention of acrolein-mediated toxicity.; Acrolein, Glutathione, Acrolein-mediated toxicity Advisors/Committee Members: Zhenquan Jia (advisor).

Subjects/Keywords: Acrolein – Toxicology; Glutathione – Metabolism

…phase II detoxification system includes glutathione (GSH) and GSH-related enzymes… …acrolein toxicity Studies have shown that GSH, glutathione-s-transferase (GST) and… …response to oxidative stress GSH is converted to its oxidative state, glutathione disulfide (… …GSSG), which regenerates reduced GSH via glutathione reductase and NADPH. About 90% of… …glutathione is present in its reduced form in the cell. While it is found in its disulfide state in…

10 more images…

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APA (6^th Edition):

Shah, H. (2013). Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism. (Masters Thesis). University of North Carolina – Greensboro. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=15055

Chicago Manual of Style (16^th Edition):

Shah, Halley. “Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism.” 2013. Masters Thesis, University of North Carolina – Greensboro. Accessed January 22, 2021. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=15055.

MLA Handbook (7^th Edition):

Shah, Halley. “Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism.” 2013. Web. 22 Jan 2021.

Vancouver:

Shah H. Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism. [Internet] [Masters thesis]. University of North Carolina – Greensboro; 2013. [cited 2021 Jan 22]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=15055.

Council of Science Editors:

Shah H. Protection of HepG2 cells from acrolein toxicity by CDDO-Im via glutathione-mediated mechanism. [Masters Thesis]. University of North Carolina – Greensboro; 2013. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=15055

McGill University

6. Jaeger, Valerie A. Glutathione S-Transferases of Rat Kidney.

Degree: PhD, Department of Pharmacology and Therapeutics, 1978, McGill University

URL: https://escholarship.mcgill.ca/downloads/1z40kw19d.pdf ; https://escholarship.mcgill.ca/concern/theses/1j92g975p

►

Les glutathion S-transférases sont une famille de protéines impliquée dans la détoxification. Les différentes transférases présentes dans le rein du rat ont été étudiées par… (more)

▼

Les glutathion S-transférases sont une famille de protéines impliquée dans la détoxification. Les différentes transférases présentes dans le rein du rat ont été étudiées par séparation isoélectrique sur gels de polyacrylamide. Cinq formes de transférase, toutes de poids moléculaire ca. 45,000, ont été trouvées dans le cytosol rénal. Deux de celles-ci correspondent aux transférases hépatiques B et M. La proportion relative des c diverses formes dépend du sexe. Les transférases rénales font voir une spécificité plus grande pour le substrat que les transférases hépatiques. Les transférases rénales sont contrôlées individuellement en ce que a) la réponse aux agents inducteurs est sélective et b) le processus de maturation de chaque transférase est distinct, même si toutes les activités atteignent leurs valeurs adultes à l’âge de 30 jours. L 'activité transférase est induite aussi prématurément qu'après la première semaine de vie et le pourcentage d'induction qui a lieu en sus du niveau de base est indépendant de l’âge. Les glutathion S-transférases rénales sont particulièrement appropriées pour l'étude de la nature et le contrôle des nombreuses enzymes hétérogènes impliquées dans le métabolisme xénobiotique.

The glutathione S-transferases are a family of proteins involved in detoxification. The different transferases in rat kidney were studied by isoelectricfocusing on polyacrylamide gels. Five forms of transferase, all of molecular weight ea. 45,000, were found in renal cytosol. Two correspond to hepatic transferases B and M. The relative proportion of the 0 various forms is sex-dependent. Renal transferases exhibit narrower substrate specificity than do hepatic transferases. The renal transferases are individually regulated in that a) response to inducing agents is selective and b) the maturational pattern of each transferase is distinct even though all activities reach adult values by age 30 days. Transferase activity is inducible as early as the first week of life and the percent induction over basal levels is not age-dependent. The renal glutathione S-transferases are particularly suitable for studying the nature and regulation of the many heterogeneous enzymes involved in xenobiotic metabolism.

Advisors/Committee Members: Neims, Allen (Supervisor).

Subjects/Keywords: Metabolism; Glutathione S-transferases

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APA (6^th Edition):

Jaeger, V. A. (1978). Glutathione S-Transferases of Rat Kidney. (Doctoral Dissertation). McGill University. Retrieved from https://escholarship.mcgill.ca/downloads/1z40kw19d.pdf ; https://escholarship.mcgill.ca/concern/theses/1j92g975p

Chicago Manual of Style (16^th Edition):

Jaeger, Valerie A. “Glutathione S-Transferases of Rat Kidney.” 1978. Doctoral Dissertation, McGill University. Accessed January 22, 2021. https://escholarship.mcgill.ca/downloads/1z40kw19d.pdf ; https://escholarship.mcgill.ca/concern/theses/1j92g975p.

MLA Handbook (7^th Edition):

Jaeger, Valerie A. “Glutathione S-Transferases of Rat Kidney.” 1978. Web. 22 Jan 2021.

Vancouver:

Jaeger VA. Glutathione S-Transferases of Rat Kidney. [Internet] [Doctoral dissertation]. McGill University; 1978. [cited 2021 Jan 22]. Available from: https://escholarship.mcgill.ca/downloads/1z40kw19d.pdf ; https://escholarship.mcgill.ca/concern/theses/1j92g975p.

Council of Science Editors:

Jaeger VA. Glutathione S-Transferases of Rat Kidney. [Doctoral Dissertation]. McGill University; 1978. Available from: https://escholarship.mcgill.ca/downloads/1z40kw19d.pdf ; https://escholarship.mcgill.ca/concern/theses/1j92g975p

7. Ogunrinu, Toyin Adeyemi. Role of the cystine-glutamate exchanger in glioma cell biology.

Degree: PhD, 2010, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,956

►

Changes in the glioma microenvironment including oxygen (O2) levels, supply of amino acid such as L-glutamate and L-cystine and glutathione (GSH) concentrations play a critical… (more)

▼

Changes in the glioma microenvironment including oxygen (O2) levels, supply of amino acid such as L-glutamate and L-cystine and glutathione (GSH) concentrations play a critical role in glioma biology. Previous data from our laboratory and others have implicated the L-cystine/L-glutamate exchanger, system xc - in the invasion and proliferation of cancers including glioma. The central aim of this dissertation was to characterize the contribution of L-cystine uptake, GSH synthesis and L-glutamate release to migration and proliferation of glioma cells. In my first study, I examined the role of system xc - mediated L-glutamate release on glioma migration. I show that activation of Ca2+ permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA-Rs) induces intracellular Ca2+ oscillations which promote migration. These findings suggest that a primary role of L-glutamate release in glioma cells is to promote migration through the autocrine and paracrine activation of Ca2+ permeable AMPA-Rs. In my second study, I examined how hypoxia affects the dependency of glioma growth on L-cystine and GSH. I show that glioma cells respond to hypoxia with increases in free radical production. When D54-MG cells were propagated under hypoxic conditions, we observed an increase in surface expression of xCT alone. I also show that hypoxia increases system xc - sensitive L-cystine uptake and consumption rates of GSH. In my last study, I examined the expression profile of xCT across high grade human glioma cell lines and in biopsied glioma samples from over 30 patients. The results show a heterogeneous expression of xCT ranging from no expression to abundant expression. Interestingly, glioma cells with minimal xCT expression no longer depend on L-cystine or GSH for growth. These studies show multiple important roles for the system xc - transporter in glioma biology.

1 online resource (xiii, 132 p. : ill., digital, PDF file)

Neurobiology;

Joint Health Sciences;

System xc- Glutamate Cystine Glioma Migration Proliferation

UNRESTRICTED

Advisors/Committee Members: Sontheimer, Harald, Nabors, L. Burt<br>, Sims, Brian<br>, Theibert, Anne<br>, Wadiche, Jacques.

Subjects/Keywords: Anoxia – metabolism<; br>; Brain Neoplasms – metabolism<; br>; Glioblastoma – metabolism<; br>; Glioma – metabolism<; br>; Glutathione – metabolism<; br>; Glutamic Acid – metabolism

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APA (6^th Edition):

Ogunrinu, T. A. (2010). Role of the cystine-glutamate exchanger in glioma cell biology. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,956

Chicago Manual of Style (16^th Edition):

Ogunrinu, Toyin Adeyemi. “Role of the cystine-glutamate exchanger in glioma cell biology.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 22, 2021. http://contentdm.mhsl.uab.edu/u?/etd,956.

MLA Handbook (7^th Edition):

Ogunrinu, Toyin Adeyemi. “Role of the cystine-glutamate exchanger in glioma cell biology.” 2010. Web. 22 Jan 2021.

Vancouver:

Ogunrinu TA. Role of the cystine-glutamate exchanger in glioma cell biology. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2021 Jan 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,956.

Council of Science Editors:

Ogunrinu TA. Role of the cystine-glutamate exchanger in glioma cell biology. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,956

University of Melbourne

8. Coventry, David Richard. The relationship between amounts of glutathione in flour and the baking quality of flour.

Degree: 1971, University of Melbourne

URL: http://hdl.handle.net/11343/114329

Subjects/Keywords: Analysis; Composition; Dough; Flour; Glutathione; Metabolism

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APA (6^th Edition):

Coventry, D. R. (1971). The relationship between amounts of glutathione in flour and the baking quality of flour. (Masters Thesis). University of Melbourne. Retrieved from http://hdl.handle.net/11343/114329

Chicago Manual of Style (16^th Edition):

Coventry, David Richard. “The relationship between amounts of glutathione in flour and the baking quality of flour.” 1971. Masters Thesis, University of Melbourne. Accessed January 22, 2021. http://hdl.handle.net/11343/114329.

MLA Handbook (7^th Edition):

Coventry, David Richard. “The relationship between amounts of glutathione in flour and the baking quality of flour.” 1971. Web. 22 Jan 2021.

Vancouver:

Coventry DR. The relationship between amounts of glutathione in flour and the baking quality of flour. [Internet] [Masters thesis]. University of Melbourne; 1971. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/11343/114329.

Council of Science Editors:

Coventry DR. The relationship between amounts of glutathione in flour and the baking quality of flour. [Masters Thesis]. University of Melbourne; 1971. Available from: http://hdl.handle.net/11343/114329

University of Arizona

9. MacFarland, Ronald Trevor. EXTRA-HEPATIC GLUTATHIONE CONJUGATION AND THE TOXICITY OF THREE HALOGENATED HYDROCARBONS.

Degree: 1982, University of Arizona

URL: http://hdl.handle.net/10150/274678

Subjects/Keywords: Halocarbons – Toxicology.; Glutathione – Metabolism.; Liver – Diseases.

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APA (6^th Edition):

MacFarland, R. T. (1982). EXTRA-HEPATIC GLUTATHIONE CONJUGATION AND THE TOXICITY OF THREE HALOGENATED HYDROCARBONS. (Masters Thesis). University of Arizona. Retrieved from http://hdl.handle.net/10150/274678

Chicago Manual of Style (16^th Edition):

MacFarland, Ronald Trevor. “EXTRA-HEPATIC GLUTATHIONE CONJUGATION AND THE TOXICITY OF THREE HALOGENATED HYDROCARBONS. ” 1982. Masters Thesis, University of Arizona. Accessed January 22, 2021. http://hdl.handle.net/10150/274678.

MLA Handbook (7^th Edition):

MacFarland, Ronald Trevor. “EXTRA-HEPATIC GLUTATHIONE CONJUGATION AND THE TOXICITY OF THREE HALOGENATED HYDROCARBONS. ” 1982. Web. 22 Jan 2021.

Vancouver:

MacFarland RT. EXTRA-HEPATIC GLUTATHIONE CONJUGATION AND THE TOXICITY OF THREE HALOGENATED HYDROCARBONS. [Internet] [Masters thesis]. University of Arizona; 1982. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10150/274678.

Council of Science Editors:

MacFarland RT. EXTRA-HEPATIC GLUTATHIONE CONJUGATION AND THE TOXICITY OF THREE HALOGENATED HYDROCARBONS. [Masters Thesis]. University of Arizona; 1982. Available from: http://hdl.handle.net/10150/274678

University of Illinois – Urbana-Champaign

10. Leslie, Matthew Thomas. Microenvironmental and metabolic influences in tumor cell redox homeostasis.

Degree: PhD, VMS - Pathobiology, 2017, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/101106

► Redox reactions dictate protein shape, regulate enzyme activity, and underscore cellular metabolism. When redox poise fails and cells are overcome by oxidation, cellular death soon… (more)

▼ Redox reactions dictate protein shape, regulate enzyme activity, and underscore cellular metabolism. When redox poise fails and cells are overcome by oxidation, cellular death soon follows. Redox biology is an especially important aspect of cancer cell biology, because oncogene-induced hyperproliferation results in pro-oxidant tumor cell phenotypes. Thus, tumor cell antioxidant systems are often inherently strained and vulnerable to further oxidative attack. Targeted therapies can be designed to kill tumor cells by pushing them beyond redox thresholds compatible with cellular life without injuring healthy cells that can more effectively dissipate oxidative stress. Radiation therapy and many chemotherapeutic drugs use this mechanism of oxidant-based cell killing to eliminate tumor cell populations. However, in clinical settings, these therapies face tumor cell resistance stemming from multifactorial changes in cellular drug and energy metabolism, environmental selective pressures, and intratumoral heterogeneity. To further advance efficacious and selective anticancer strategies, increased understanding of microenvironmental and metabolic influences in tumor cells redox homeostasis is needed. Poorly arranged and malfunctioning vasculature in the tumor microenvironment causes heterogeneous regions of hypoxia to form throughout the solid mass. Clinically, tumor hypoxia is a negative prognostic indicator for a more aggressive phenotype and is associated with treatment resistance. Metabolically, tumor hypoxia results in hypoxia inducible factor-driven gene network activation and enhanced mitochondrial production of reactive oxygen species. Given this, it is important to match laboratory in vitro studies as closely as possible to the in vivo conditions of the tumor microenvironment. However, even simple in vitro hypoxic studies are complicated by the rigors of hypoxic experimentation and, thus, most studies are conducted at hyperoxic atmospheric levels of oxygen. Engineered microfluidic platforms offer an approach to hypoxic laboratory studies. This report validates an ease-of-use platform suitable to study complex cell behaviors in hypoxia. Herein we present the design and implementation of an open-well microfluidic platform that enables on-chip cell culture, experimentation, and microscopy in a controlled hypoxic microenvironment. This platform has been theoretically and experimentally validated to quickly induce and maintain 0.3 mg/L O2 hypoxia, and it has enabled studies of the stabilization of hypoxia inducible factor in hypoxia and the redox response of the mitochondrial matrix in hypoxia. The glutathione system functions in antioxidant defense and xenobiotic detoxification to preserve subcellular redox poise and maintain enzymes in functional reduced states. Glutathione is produced from its constitutive amino acids in a two-step enzymatic process that occurs in the cytosol. Despite glutathione’s role in cellular antioxidant defense, its production in the pro-oxidant state of hypoxia has been under studied. We… Advisors/Committee Members: Gaskins, H. Rex (advisor), Gaskins, H. Rex (Committee Chair), Kenis, Paul (committee member), Kulenschmidt, Mark (committee member), Lau, Gee (committee member), Fan, Tim (committee member), Grippo, Paul (committee member).

Subjects/Keywords: Cancer; RAS Oncogene; Metabolism; Glutaminolysis; Glutamine; Alpha-ketoglutarate; Glutathione; GSH; Redox; Reactive Oxygen Species; Hypoxia; Microfluidics; roGFP2 biosensor

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APA (6^th Edition):

Leslie, M. T. (2017). Microenvironmental and metabolic influences in tumor cell redox homeostasis. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/101106

Chicago Manual of Style (16^th Edition):

Leslie, Matthew Thomas. “Microenvironmental and metabolic influences in tumor cell redox homeostasis.” 2017. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 22, 2021. http://hdl.handle.net/2142/101106.

MLA Handbook (7^th Edition):

Leslie, Matthew Thomas. “Microenvironmental and metabolic influences in tumor cell redox homeostasis.” 2017. Web. 22 Jan 2021.

Vancouver:

Leslie MT. Microenvironmental and metabolic influences in tumor cell redox homeostasis. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2017. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2142/101106.

Council of Science Editors:

Leslie MT. Microenvironmental and metabolic influences in tumor cell redox homeostasis. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2017. Available from: http://hdl.handle.net/2142/101106

Texas Tech University

11. Chung, Cha Kwon. Identification of methionine as a possible precursor to the selenocysteine catalytic site of glutathione peroxidase.

Degree: Home Economics, 1985, Texas Tech University

URL: http://hdl.handle.net/2346/14451

Subjects/Keywords: Selenocysteine; Selenium in animal nutrition; Selenium – Metabolism; Peroxidase; Glutathione

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APA (6^th Edition):

Chung, C. K. (1985). Identification of methionine as a possible precursor to the selenocysteine catalytic site of glutathione peroxidase. (Thesis). Texas Tech University. Retrieved from http://hdl.handle.net/2346/14451

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chung, Cha Kwon. “Identification of methionine as a possible precursor to the selenocysteine catalytic site of glutathione peroxidase.” 1985. Thesis, Texas Tech University. Accessed January 22, 2021. http://hdl.handle.net/2346/14451.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chung, Cha Kwon. “Identification of methionine as a possible precursor to the selenocysteine catalytic site of glutathione peroxidase.” 1985. Web. 22 Jan 2021.

Vancouver:

Chung CK. Identification of methionine as a possible precursor to the selenocysteine catalytic site of glutathione peroxidase. [Internet] [Thesis]. Texas Tech University; 1985. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2346/14451.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chung CK. Identification of methionine as a possible precursor to the selenocysteine catalytic site of glutathione peroxidase. [Thesis]. Texas Tech University; 1985. Available from: http://hdl.handle.net/2346/14451

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of South Carolina

12. Ozer, Hatice Kubra. The Role of Intermembrane Space Redox Factors In Glutathione Metabolism And Intracellular Redox Equilibrium.

Degree: PhD, Chemistry and Biochemistry, 2015, University of South Carolina

URL: https://scholarcommons.sc.edu/etd/3702

► The mitochondrial intermembrane space (IMS) is a unique subcellular compartment that houses key thiol-dependent redox pathways such as protein transport, mitochondrial respiration, and detoxification… (more)

▼ The mitochondrial intermembrane space (IMS) is a unique subcellular compartment that houses key thiol-dependent redox pathways such as protein transport, mitochondrial respiration, and detoxification of ROS (reactive oxygen species). These pathways are all dependent on cysteine-rich proteins, thus maintaining thiol-disulfide balance in this organelle is crucial for cellular functions. An IMS protein import pathway called the Mia40-Erv1 disulfide relay system uses disulfide bond formation for the import and retention of substrate proteins in the IMS. Erv1 is also suggested to be involved in maturation of cytosolic Fe-S cluster proteins and regulation of iron homeostasis in S. cerevisiae. However, these studies were performed on one particular erv1 mutant strain (named as erv1-1) that we discovered has additional defects in glutathione (GSH) metabolism due to a secondary mutation in the gene encoding the GSH biosynthesis enzyme, Gsh1. Since the tripeptide GSH is also required for iron homeostasis and cytosolic Fe-S protein biogenesis, the Erv1-dependent connection between mitochondrial protein import, GSH metabolism, and iron homeostasis was investigated in several erv1 mutants. The GSH depletion phenotype was only detected in the erv1-1 strain and could be rescued by expressing GSH1 or adding GSH to the growth media. Additionally, expression of the iron uptake gene, FET3 and enzyme activities of Fe-S cluster proteins in several erv1 mutants were tested. Only the erv1-1 mutant has an iron misregulation defect, which could be rescued with GSH addition, and no significant effects on Fe-S cluster protein activities were detected. Our data suggests that the defects of cytosolic Fe-S maturation and iron regulation first reported in the erv1-1 strain is a direct consequence of GSH depletion rather than indicating a direct role for Erv1 in iron metabolism and cytosolic Fe-S cluster biogenesis. We also characterized how mutations of Mia40 influence GSH metabolism and GSH:GSSG pools in the cytosol, mitochondrial matrix and intermembrane space. We have found that defects in Mia40 only influence the IMS redox state and do not alter cellular GSH levels. Additionally, we determined that defects in Mia40 do not impact iron homeostasis or Fe-S cluster biogenesis. Furthermore, utilizing the roGFP2 in vivo sensors, we demonstrated how the deletion of manganese cofactor of superoxide dismutase 2 transporter Mtm1 and the citrate-oxoglutarate carrier Yhm2 affect the redox status of the mitochondrial matrix and IMS and cellular GSH levels. Deletion of MTM1 only leads to a large oxidative shift in the IMS GSH:GSSG redox state. In the contrary, deletion of YHM2 shows a smaller effect on the mitochondrial GSH:GSSG redox state even though, both mtm1Δ and yhm2Δ mutants were shown to have reduced mitochondrial GSH levels. Overall, we successfully characterized the roles of Erv1 and Mia40 in GSH metabolism, mitochondrial import and subcellular redox state which hereby helps to reveal their roles in Fe-S cluster biogenesis and… Advisors/Committee Members: Caryn E. Outten.

Subjects/Keywords: Chemistry; Physical Sciences and Mathematics; Role of Intermembrane; Space Redox Factors; Glutathione; Metabolism; Intracellular Redox; Equilibrium

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APA (6^th Edition):

Ozer, H. K. (2015). The Role of Intermembrane Space Redox Factors In Glutathione Metabolism And Intracellular Redox Equilibrium. (Doctoral Dissertation). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/3702

Chicago Manual of Style (16^th Edition):

Ozer, Hatice Kubra. “The Role of Intermembrane Space Redox Factors In Glutathione Metabolism And Intracellular Redox Equilibrium.” 2015. Doctoral Dissertation, University of South Carolina. Accessed January 22, 2021. https://scholarcommons.sc.edu/etd/3702.

MLA Handbook (7^th Edition):

Ozer, Hatice Kubra. “The Role of Intermembrane Space Redox Factors In Glutathione Metabolism And Intracellular Redox Equilibrium.” 2015. Web. 22 Jan 2021.

Vancouver:

Ozer HK. The Role of Intermembrane Space Redox Factors In Glutathione Metabolism And Intracellular Redox Equilibrium. [Internet] [Doctoral dissertation]. University of South Carolina; 2015. [cited 2021 Jan 22]. Available from: https://scholarcommons.sc.edu/etd/3702.

Council of Science Editors:

Ozer HK. The Role of Intermembrane Space Redox Factors In Glutathione Metabolism And Intracellular Redox Equilibrium. [Doctoral Dissertation]. University of South Carolina; 2015. Available from: https://scholarcommons.sc.edu/etd/3702

University of Helsinki

13. Hovinen, Topi. Metabolic Consequences of Folate Deficiency in Mice.

Degree: Medicinska fakulteten, 2016, University of Helsinki

URL: http://hdl.handle.net/10138/174414

► Folate deficiency (FD) has been found to cause number of medical conditions varying from megaloblastic anemia to fetal neural tube defects but the molecular basis… (more)

Subjects/Keywords: folate; metabolism; cysteine; glutathione; taurine; bile acids; Obstetrics and Gynecology; Naistentaudit ja synnytykset; Molekyylineurologia; Kvinnosjukdomar och förlossningar

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APA (6^th Edition):

Hovinen, T. (2016). Metabolic Consequences of Folate Deficiency in Mice. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/174414

Chicago Manual of Style (16^th Edition):

Hovinen, Topi. “Metabolic Consequences of Folate Deficiency in Mice.” 2016. Masters Thesis, University of Helsinki. Accessed January 22, 2021. http://hdl.handle.net/10138/174414.

MLA Handbook (7^th Edition):

Hovinen, Topi. “Metabolic Consequences of Folate Deficiency in Mice.” 2016. Web. 22 Jan 2021.

Vancouver:

Hovinen T. Metabolic Consequences of Folate Deficiency in Mice. [Internet] [Masters thesis]. University of Helsinki; 2016. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10138/174414.

Council of Science Editors:

Hovinen T. Metabolic Consequences of Folate Deficiency in Mice. [Masters Thesis]. University of Helsinki; 2016. Available from: http://hdl.handle.net/10138/174414

14. Robert, Stephanie Marie. Cystine/glutamate Transporters As Prognostic & Therapeutic Markers Of Primary Brain Tumors.

Degree: 2012, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1791

►

Glioblastoma multiforme (GBM) are the most prevalent and aggressive malignant brain tumors. Current treatment - a combination of radiation, chemotherapy and resection - has limited… (more)

▼

Glioblastoma multiforme (GBM) are the most prevalent and aggressive malignant brain tumors. Current treatment - a combination of radiation, chemotherapy and resection - has limited effectiveness and offers poor prognosis. In this study, we examined the roles of system xc- (SXC) and excitatory amino acid transporters (EAATs), which transport the amino acids cystine and glutamate, on tumor growth, neurotoxicity, and peritumoral seizure activity. Tissue micro-arrays from 45 patients were examined by immuno-histochemistry, comparing tumor-bearing tissue and adjacent normal brain. Using a novel flank tumor propagation technique, we chose 3 glioma samples with varying SXC and EAAT expression levels to study their physiological differences using cell and tissue assays. Examination of patient tissues indicated glioma patients can be stratified into high or low level system xc- expressers, compared to normal brain. In low SXC expressing tumors, cystine uptake assays suggested an alternative transporter supplying intracellular cystine for GSH synthesis and redox protection; EAAT1 and EAAT3 were discovered to mediate this alternative transport. High SXC expression correlated with increased proliferation over 5 days, neurotoxicity in 48 and 72 hour glioma/neuron co-cultures, and a significant 67.8% increase in seizure prevalence upon intracranial implantation in vivo. Furthermore, system xc- inhibition using Sulfasalazine, an FDA approved drug, resulted in decreased proliferation of all tumor lines expressing SXC, and decreased cystine uptake and neurotoxicity in tumor lines expressing high levels of SXC and no EAATs, during the same time points. Our results suggest that SXC should be further investigated as a prognostic marker for tumor growth and seizure activity as well as a therapeutic marker for glioblastoma patients, as our data argues for adjuvant Sulfasalazine administration in patients with glioblastomas expressing SXC.

MSBMS

1 online resource (ix, 60 pages) :illustrations

M.S.University of Alabama at Birmingham2012.

Joint Health Sciences

Excitatory Amino Acid Transporters (EAAT) Glioblastoma Multiforme (GBM) Glutathione (GSH) Seizures Sulfasalazine (SAS) System xc- (SXC)

UNRESTRICTED

Advisors/Committee Members: Harald Sontheimer, Nabors,Burt Olsen,Michelle Smith,Peter.

Subjects/Keywords: Amino Acid Transport System X-AG – metabolism.<; br>; Brain Neoplasms – metabolism<; br>; Glioblastoma.<; br>; Glutathione<; br>; Seizures<; br>; Sulfasalazine.

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APA (6^th Edition):

Robert, S. M. (2012). Cystine/glutamate Transporters As Prognostic & Therapeutic Markers Of Primary Brain Tumors. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1791

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Robert, Stephanie Marie. “Cystine/glutamate Transporters As Prognostic & Therapeutic Markers Of Primary Brain Tumors.” 2012. Thesis, University of Alabama – Birmingham. Accessed January 22, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1791.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Robert, Stephanie Marie. “Cystine/glutamate Transporters As Prognostic & Therapeutic Markers Of Primary Brain Tumors.” 2012. Web. 22 Jan 2021.

Vancouver:

Robert SM. Cystine/glutamate Transporters As Prognostic & Therapeutic Markers Of Primary Brain Tumors. [Internet] [Thesis]. University of Alabama – Birmingham; 2012. [cited 2021 Jan 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1791.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Robert SM. Cystine/glutamate Transporters As Prognostic & Therapeutic Markers Of Primary Brain Tumors. [Thesis]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1791

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University

15. Thompson, Lawrence Casper. Dynamic, Structural, and Mechanistic Study of Glutathione Transferases.

Degree: PhD, Biochemistry, 2006, Vanderbilt University

URL: http://hdl.handle.net/1803/12667

► This project involved the investigation of both the dynamic features of the dimer interface of the Mu class GSH transferase rGSTM1-1, as well as, the… (more)

Subjects/Keywords: hcca isomerase; hydrogen-deuterium exchange mass spectrometry; glutathione cofactor; isomerization; glutathione binding; mechanistic enzymology; transient state kinetics; crystallography; naphthalene metabolism; Xenobiotics – Metabolism; phase II enzymes; xenobiotic catabolism; kappa glutathione transferases; dimer stability; Glutathione transferase

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Thompson, L. C. (2006). Dynamic, Structural, and Mechanistic Study of Glutathione Transferases. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12667

Chicago Manual of Style (16^th Edition):

Thompson, Lawrence Casper. “Dynamic, Structural, and Mechanistic Study of Glutathione Transferases.” 2006. Doctoral Dissertation, Vanderbilt University. Accessed January 22, 2021. http://hdl.handle.net/1803/12667.

MLA Handbook (7^th Edition):

Thompson, Lawrence Casper. “Dynamic, Structural, and Mechanistic Study of Glutathione Transferases.” 2006. Web. 22 Jan 2021.

Vancouver:

Thompson LC. Dynamic, Structural, and Mechanistic Study of Glutathione Transferases. [Internet] [Doctoral dissertation]. Vanderbilt University; 2006. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1803/12667.

Council of Science Editors:

Thompson LC. Dynamic, Structural, and Mechanistic Study of Glutathione Transferases. [Doctoral Dissertation]. Vanderbilt University; 2006. Available from: http://hdl.handle.net/1803/12667

16. 広田, 孝司. グルタチオン代謝におけるデヒドロペプチダーゼ-Iの役割に関する研究 : Role of dehydropeptidase-I in the metabolism of glutathione.

Degree: Chiba University / 千葉大学

URL: http://opac.ll.chiba-u.jp/da/curator/900047121/

研究科: 千葉大学大学院薬学研究院

修了年:1988

学位:千大院薬博乙第53号

Advisors/Committee Members: 千葉大学大学院薬学研究院.

Subjects/Keywords: dehydropeptidase-Ⅰ; DHP-Ⅰ; glutathione; metabolism; デヒドロペプチダーゼ-Ⅰ; グルタチオン; 代謝

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APA (6^th Edition):

広田, �. (n.d.). グルタチオン代謝におけるデヒドロペプチダーゼ-Iの役割に関する研究 : Role of dehydropeptidase-I in the metabolism of glutathione. (Thesis). Chiba University / 千葉大学. Retrieved from http://opac.ll.chiba-u.jp/da/curator/900047121/

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

広田, 孝司. “グルタチオン代謝におけるデヒドロペプチダーゼ-Iの役割に関する研究 : Role of dehydropeptidase-I in the metabolism of glutathione.” Thesis, Chiba University / 千葉大学. Accessed January 22, 2021. http://opac.ll.chiba-u.jp/da/curator/900047121/.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

広田, 孝司. “グルタチオン代謝におけるデヒドロペプチダーゼ-Iの役割に関する研究 : Role of dehydropeptidase-I in the metabolism of glutathione.” Web. 22 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

広田 �. グルタチオン代謝におけるデヒドロペプチダーゼ-Iの役割に関する研究 : Role of dehydropeptidase-I in the metabolism of glutathione. [Internet] [Thesis]. Chiba University / 千葉大学; [cited 2021 Jan 22]. Available from: http://opac.ll.chiba-u.jp/da/curator/900047121/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

広田 �. グルタチオン代謝におけるデヒドロペプチダーゼ-Iの役割に関する研究 : Role of dehydropeptidase-I in the metabolism of glutathione. [Thesis]. Chiba University / 千葉大学; Available from: http://opac.ll.chiba-u.jp/da/curator/900047121/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

17. Pinto, Sheila Serra Vieira. Estudo complementar da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis.

Degree: Mestrado, Fisiopatologia Experimental, 2009, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5160/tde-15042009-145222/ ;

►

Sabe-se que a atividade da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis é cerca de 15 a 20 vezes a encontrada nos eritrócitos humanos.… (more)

▼

Sabe-se que a atividade da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis é cerca de 15 a 20 vezes a encontrada nos eritrócitos humanos. Pretendendo-se investigar se esta hiperatividade também se encontra ou não aumentada nas outras enzimas eritrocitárias, levou-se a efeito a dosagem das atividades das enzimas glicolíticas bem de outras enzimas relacionadas ao metabolismo óxido-redutor do eritrócito do marsupial. Alguns dados bioquímicos sorológicos, hematológicos e imunológicos foram também obtidos. Assim sendo, as seguintes enzimas eritrocitárias foram estudadas: hexoquinase, glicose fosfato isomerase, fosfofrutoquinase, aldolase, triose fosfato isomerase, gliceraldeido-3-fosfato desidrogenase, fosfogliceratoquinase, difosfoglicerato mutase, monofosfoglicerato mutase, enolase, piruvato quinase, lactato desidrogenase, glicose-6-fosfato desidrogenase, 6-fosfogliconato desidrogenase, glutationa redutase, glutationa peroxidase, glutationa S-transferase, nicotinamida adenina dinucleotideo fosfato diaforase, nicotinamida adenina dinucleotideo meta-hemoglobina redutase, superóxido dismutase, aspartato aminotransferase, adenilato quinase, adenosina desaminase e acetilcolinesterase. Embora a maioria das enzimas estudadas tenham revelado atividades semelhantes às encontradas nos eritrócitos humanos, foram observados aumentos significativos da hexoquinase, piruvato quinase e glutationa S-transferase. Entretanto, a atividade da glutationa peroxidase apresentou grande aumento de atividade, cerca de dez a doze vezes a encontrada nos eritrócitos humanos, talvez agindo em conjunto com a hiperatividade da glicose-6-fosfato desidrogenase da ordem de dez a quinze vezes já descrita nos eritrócitos humanos

It is known that erythrocyte glucose-6-phosphate dehydrogenase specific activity of Didelphis marsupialis is about 15-20 times higher than human red cells. In order to investigate whether this hyperactivity is extended or not to other red cell enzymes, it was proposed to ascertain the activity of the glycolytic enzymes as well as other related to the redox metabolism of the opossum erythrocyte. Some biochemical, hematological and immunological data were also assayed as well. That being so, the following red cell enzymes were assayed: hexokinase, glucose phosphate isomerase, phosphofructokinase, aldolase, triose phosphate isomerase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate kinase, diphosphoglycerate mutase, monophosphoglycerate mutase, enolase, pyruvate kinase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, glutathione reductase, glutathione peroxidase, glutathione S-transferase, nicotinamide adenine dinucleotide phosphate diaphorase, nicotinamide adenine dinucleotide metahemoglobin reductase, superoxide dismutase, aspartate amino-transferase, adenylate kinase, adenosine deaminase and acetylcholinesterase . Although most of the enzymatic activities disclosed to be similar to humans, some enzymes exhibited high activities as…

Advisors/Committee Members: Barretto, Orlando Cesar de Oliveira.

Subjects/Keywords: Clinical enzyme tests; Didelphis; Didelphis; Energy metabolism; Ensaios enzimáticos clínicos; Glucose-6-fosfato desidrogenase; Glucosephosphate dehydrogenase; Glutathione peroxidase; Glutationa peroxidase; Metabolismo energético

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APA (6^th Edition):

Pinto, S. S. V. (2009). Estudo complementar da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5160/tde-15042009-145222/ ;

Chicago Manual of Style (16^th Edition):

Pinto, Sheila Serra Vieira. “Estudo complementar da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis.” 2009. Masters Thesis, University of São Paulo. Accessed January 22, 2021. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-15042009-145222/ ;.

MLA Handbook (7^th Edition):

Pinto, Sheila Serra Vieira. “Estudo complementar da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis.” 2009. Web. 22 Jan 2021.

Vancouver:

Pinto SSV. Estudo complementar da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis. [Internet] [Masters thesis]. University of São Paulo; 2009. [cited 2021 Jan 22]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5160/tde-15042009-145222/ ;.

Council of Science Editors:

Pinto SSV. Estudo complementar da glicose-6-fosfato desidrogenase eritrocitária do marsupial brasileiro Didelphis marsupialis. [Masters Thesis]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/5/5160/tde-15042009-145222/ ;

Lincoln University

18. Burd, Anna Mae. In vivo and in vitro studies of 4-vinylcyclohexene diepoxide in wild-caught female brushtail possums (Trichosurus vulpecula) and Norway rats (Rattus norvegicus) and its potential as a fertility control agent.

Degree: 2014, Lincoln University

URL: http://hdl.handle.net/10182/5951

► In New Zealand (NZ), the brushtail possum (Trichosurus vulpecula) poses a major threat to native flora and fauna and it is the main wildlife vector… (more)

▼ In New Zealand (NZ), the brushtail possum (Trichosurus vulpecula) poses a major threat to native flora and fauna and it is the main wildlife vector for bovine tuberculosis. Primary control utilizes lethal means but these methods have limited efficacy long-term and are associated with environmental impact concerns. Fertility control has become more popular as it is potentially more effective, sustainable and humane. The industrial chemical, 4-vinylcyclohexene diepoxide (VCD) may serve as an ideal chemosterilant candidate for investigation. Oral gavage studies have shown that VCD reduces the pool of non-regenerating immature ovarian follicles in rodents, resulting in premature ovarian failure and sterility. The first objective of these studies was to examine the effects of orally administered VCD on female possum ovarian follicle populations. Orally delivered VCD had no effect on the primordial follicles of adult female possums and two formulations aimed at improving VCD uptake and efficacy did not change this outcome. The second objective examined the uptake and metabolism of orally administered VCD in female possums and rats in vivo. VCD concentration in the blood of rats was significantly greater than in possums while concentrations of VCD in the stomach were comparable between species. VCD dosing did not alter pH of stomach contents of possums while that of rats was increased and sustained for 6 hours. VCD-induced reductions in ovarian and liver glutathione levels were observed in the rat with no effects in the possum. It was determined that the highly acidic environment of the stomach of possums poses an initial barrier for orally delivered VCD. Without sufficient quantities of VCD reaching the liver and ovaries of possums, it was not possible to compare species differences in metabolism in vivo. The third objective examined the fate of VCD when exposed to acidic environments and stomach contents and the effects of VCD on liver metabolism in vitro in possums and rats. VCD hydrolysis in stomach contents was slower in possums compared with rats suggesting that possum stomach contents are able to retain VCD longer, thus potentially modulating VCD toxicity. GSH levels in possum liver tissue were less affected when incubated with VCD compared with rats, suggesting an increased detoxifying capacity of possums. Preliminary data on the ability of possum liver microsomes to convert VCD’s parent compound, 4-vinycyclohexene, to VCD corroborated the GSH findings. Collectively, these findings suggest that VCD may not be suitable for possum fertility control when delivered orally in a raw unprotected chemical state. Encapsulation of VCD with an additional active compound, triptolide, is being examined as a novel chemosterilant (ContraPest®, SenesTech®, Flagstaff, Arizona). The fourth objective examined ContraPest® efficacy in wild-caught female Norway rats. The ovarian primordial follicle pools of ContraPest®-consuming rats were reduced compared with controls. The proposed protection of the active components within ContraPest®…

Subjects/Keywords: Brushtail possum; Norway rat; fertility control; pest control; chemosterilant; bait; 4-vinylcyclohexene diepoxide; ovary; ovarian follicle; stomach pH; glutathione; metabolism; 06 Biological Sciences; 070201 Animal Breeding

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APA (6^th Edition):

Burd, A. M. (2014). In vivo and in vitro studies of 4-vinylcyclohexene diepoxide in wild-caught female brushtail possums (Trichosurus vulpecula) and Norway rats (Rattus norvegicus) and its potential as a fertility control agent. (Thesis). Lincoln University. Retrieved from http://hdl.handle.net/10182/5951

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Burd, Anna Mae. “In vivo and in vitro studies of 4-vinylcyclohexene diepoxide in wild-caught female brushtail possums (Trichosurus vulpecula) and Norway rats (Rattus norvegicus) and its potential as a fertility control agent.” 2014. Thesis, Lincoln University. Accessed January 22, 2021. http://hdl.handle.net/10182/5951.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Burd, Anna Mae. “In vivo and in vitro studies of 4-vinylcyclohexene diepoxide in wild-caught female brushtail possums (Trichosurus vulpecula) and Norway rats (Rattus norvegicus) and its potential as a fertility control agent.” 2014. Web. 22 Jan 2021.

Vancouver:

Burd AM. In vivo and in vitro studies of 4-vinylcyclohexene diepoxide in wild-caught female brushtail possums (Trichosurus vulpecula) and Norway rats (Rattus norvegicus) and its potential as a fertility control agent. [Internet] [Thesis]. Lincoln University; 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10182/5951.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Burd AM. In vivo and in vitro studies of 4-vinylcyclohexene diepoxide in wild-caught female brushtail possums (Trichosurus vulpecula) and Norway rats (Rattus norvegicus) and its potential as a fertility control agent. [Thesis]. Lincoln University; 2014. Available from: http://hdl.handle.net/10182/5951

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. McGurn, Leah. Secoisolariciresinol (SECO) analogues: oxidative metabolism, cytochrome P450 inhibition and implications for toxicity.

Degree: 2016, University of Saskatchewan

URL: http://hdl.handle.net/10388/ETD-2016-02-2434

► Secoisolariciresinol (SECO) is the major lignan present in flaxseed, but unlike the structurally related lignan nordihydroguaiaretic acid, it is not associated with toxicity. The major… (more)

▼ Secoisolariciresinol (SECO) is the major lignan present in flaxseed, but unlike the structurally related lignan nordihydroguaiaretic acid, it is not associated with toxicity. The major phase I metabolite of SECO is lariciresinol, likely formed as a result of para-quinone methide (p-QM) formation followed by an intramolecular cyclization, thereby minimizing any toxicity associated with the p-QM. Four analogues of SECO were used to investigate substituent effects on lignan metabolism and formation of reactive quinones. HPLC methods were developed for analysis of SECO analogues and their metabolites. The stability of SECO analogues (1 mM) in a 50 mM Na2HPO4 buffer at pH 6.0 and 7.4 were quantified. Enzymatic oxidation experiments using mushroom tyrosinase and microsomes harvested from male Sprague-Dawley rats were performed with and without a GSH trapping system. Mass spectrometry and LC-MS were used to identify metabolites. Life Technologies was contracted to perform IC50 inhibition assays on SECO and the SECO analogues against CYP3A4, CYP3A5, CYP2C9 and CYP2C19 cytochrome P450 isoforms. All SECO analogues were stable at pH 6.0. SECO-2 was stable at pH 7.4 but SECO-1, -3 and -4 were unstable at pH 7.4. Autoxidation of SECO -1, -3 and -4 were 1st order reactions with t1/2 of 9.0 h, 1.7 h and 7.0 h respectively. Mushroom tyrosinase oxidations were performed to generate ortho-quinone standards. SECO-1 -3 and -4 were oxidized by mushroom tyrosinase but SECO-2 was not. Trapping with GSH produces aromatic ring conjugates for SECO-1, -3, -4. Results from microsomal oxidations for SECO-1, -3 and -4 are consistent with these standards. SECO-2 was metabolized by a microsomal system to produce a benzyl GSH adduct. Dealkylation products were also observed. All SECO analogues formed quinones but interestingly, GSH conjugation was competitive with intramolecular cyclization. All cytochrome P450 isoforms were inhibited by every analogue tested to varying degrees, a potential cause of toxicity concerns. Quinones are known to cause toxicity in vivo, including cytotoxicity, immunotoxicity, and carcinogenesis. Our results suggest that since the phenol and catechol lignans form GSH adducts in addition to intramolecular cyclization products, this class of lignans have the potential to cause toxicity. Advisors/Committee Members: Krol, Ed S., Weber, Lynn P., Jones, Paul D., Low, Nicholas H..

Subjects/Keywords: secoisolariciresinol; lignans; xenobiotic metabolism; quinones; reactive metabolites; glutathione conjugates; hepatotoxicity

…2.6.3 Metabolism-based drug-drug interactions… …17 2.9 Xenobiotic Metabolism… …18 2.9.2 Phase I metabolism… …20 2.9.2.1.3 Cytochrome P450 metabolism… …20 2.9.2.1.4 Cytochrome P450 metabolism and bioactivation…

15 more images…

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APA (6^th Edition):

McGurn, L. (2016). Secoisolariciresinol (SECO) analogues: oxidative metabolism, cytochrome P450 inhibition and implications for toxicity. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/ETD-2016-02-2434

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

McGurn, Leah. “Secoisolariciresinol (SECO) analogues: oxidative metabolism, cytochrome P450 inhibition and implications for toxicity.” 2016. Thesis, University of Saskatchewan. Accessed January 22, 2021. http://hdl.handle.net/10388/ETD-2016-02-2434.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

McGurn, Leah. “Secoisolariciresinol (SECO) analogues: oxidative metabolism, cytochrome P450 inhibition and implications for toxicity.” 2016. Web. 22 Jan 2021.

Vancouver:

McGurn L. Secoisolariciresinol (SECO) analogues: oxidative metabolism, cytochrome P450 inhibition and implications for toxicity. [Internet] [Thesis]. University of Saskatchewan; 2016. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10388/ETD-2016-02-2434.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

McGurn L. Secoisolariciresinol (SECO) analogues: oxidative metabolism, cytochrome P450 inhibition and implications for toxicity. [Thesis]. University of Saskatchewan; 2016. Available from: http://hdl.handle.net/10388/ETD-2016-02-2434

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

20. Riegel, Gilles. Rôle de la voie du stress du réticulum et de la biosynthèse du glutathion dans l’activité anticancéreuse de composés organométalliques à base de ruthénium dans le cancer gastrique : Role of the ER stress and glutathione biosynthesis pathway in the anticancer activity of organometallic ruthenium-based compounds for the treatment of gastric cancer.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2019, Université de Strasbourg

URL: http://www.theses.fr/2019STRAJ071

►

Le traitement du cancer repose sur une résection chirurgical associée à une chimiothérapie péri-opératoire à base de platine. Ces drogues provoquent des effets secondaires et… (more)

▼

Le traitement du cancer repose sur une résection chirurgical associée à une chimiothérapie péri-opératoire à base de platine. Ces drogues provoquent des effets secondaires et sont sensibles à des mécanismes de résistances, soulignant la nécessité de développer de nouvelles thérapies parmi lesquelles les dérivés de ruthénium démontrent des propriétés prometteuses.Ce travail démontre le rôle du métabolisme, notamment des voies de transsulfuration et de la biosynthèse de glutathion dans l’activité du RDC11 (ruthenium derived compounds). Ces dérégulations métaboliques sont médiées par l’effet du RDC11 sur la voie du stress du réticulum. En outre, j’ai caractérisé le rôle de l’atome métallique dans la sensibilité des cellules cancéreuses face à ces composés. Le remplacement d’un atome de ruthénium par un atome d’osmium réduit significativement l’efflux de ces composés, augmentant leur concentration intracellulaire et leur efficacité.Ces travaux caractérisent le rôle du métabolisme pour l’activité des dérivés organométalliques, ouvrant de nouvelles perspectives pour l’étude de leur mode d’action, visant à favoriser l’entrée de ceux-ci en essai clinique.

Cancer treatment is still based on surgery associated with platinum-based chemotherapy. These drugs induce side effects and are sensitive to resistance mechanisms. This shows the need to develop new anticancer therapies among which ruthenium compounds display promising properties.This study demonstrates the implication of metabolism, namely, the transsulfuration pathway and glutathione biosynthesis in the activity of the RDC11 (ruthenium derived compounds). These metabolic regulations are mediated by the effect of RDC11 on the ER stress pathway. Furthermore, I characterized the role of the metallic atoms in the sensitivity of cancer cells towards these drugs. More precisely, replacement of ruthenium by osmium reduces strongly the efflux of these drugs, increasing their intracellular concentration and efficiency.This work characterises the role of cellular metabolism for the anticancer activity of organometallic compounds, opening the way for the investigation of these compounds mode of action looking forward entry in clinical trials.

Advisors/Committee Members: Mellitzer, Georg (thesis director), Gaiddon, Christian (thesis director).

Subjects/Keywords: Stress du réticulum; Métabolisme; Efflux; Composés organométalliques; Biosynthèse du glutathion; Transsulfuration; Reticulum stress; Metabolism; Efflux; Organometallic compounds; Glutathione biosynthesis; Transsulfuration; 616.99; 615.7

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Riegel, G. (2019). Rôle de la voie du stress du réticulum et de la biosynthèse du glutathion dans l’activité anticancéreuse de composés organométalliques à base de ruthénium dans le cancer gastrique : Role of the ER stress and glutathione biosynthesis pathway in the anticancer activity of organometallic ruthenium-based compounds for the treatment of gastric cancer. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2019STRAJ071

Chicago Manual of Style (16^th Edition):

Riegel, Gilles. “Rôle de la voie du stress du réticulum et de la biosynthèse du glutathion dans l’activité anticancéreuse de composés organométalliques à base de ruthénium dans le cancer gastrique : Role of the ER stress and glutathione biosynthesis pathway in the anticancer activity of organometallic ruthenium-based compounds for the treatment of gastric cancer.” 2019. Doctoral Dissertation, Université de Strasbourg. Accessed January 22, 2021. http://www.theses.fr/2019STRAJ071.

MLA Handbook (7^th Edition):

Riegel, Gilles. “Rôle de la voie du stress du réticulum et de la biosynthèse du glutathion dans l’activité anticancéreuse de composés organométalliques à base de ruthénium dans le cancer gastrique : Role of the ER stress and glutathione biosynthesis pathway in the anticancer activity of organometallic ruthenium-based compounds for the treatment of gastric cancer.” 2019. Web. 22 Jan 2021.

Vancouver:

Riegel G. Rôle de la voie du stress du réticulum et de la biosynthèse du glutathion dans l’activité anticancéreuse de composés organométalliques à base de ruthénium dans le cancer gastrique : Role of the ER stress and glutathione biosynthesis pathway in the anticancer activity of organometallic ruthenium-based compounds for the treatment of gastric cancer. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2019. [cited 2021 Jan 22]. Available from: http://www.theses.fr/2019STRAJ071.

Council of Science Editors:

Riegel G. Rôle de la voie du stress du réticulum et de la biosynthèse du glutathion dans l’activité anticancéreuse de composés organométalliques à base de ruthénium dans le cancer gastrique : Role of the ER stress and glutathione biosynthesis pathway in the anticancer activity of organometallic ruthenium-based compounds for the treatment of gastric cancer. [Doctoral Dissertation]. Université de Strasbourg; 2019. Available from: http://www.theses.fr/2019STRAJ071

Université Paris-Sud – Paris XI

21. Narainsamy, Kinsley. Biologie systémique de la résistance au stress oxydant métabolique : rôles du glutathion, du méthylglyoxal et des glyoxalases : System biology of the metabolic oxydative stress resistance : role of glutathione, methylglyoxal and glyoxalases.

Degree: Docteur es, Biologie, 2012, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2012PA112099

► Apparues il y a environ trois milliards d'années, les cyanobactéries ont façonné notre planète, en produisant l’atmosphère oxygénique. De nos jours, les cyanobactéries sont les… (more)

▼ Apparues il y a environ trois milliards d'années, les cyanobactéries ont façonné notre planète, en produisant l’atmosphère oxygénique. De nos jours, les cyanobactéries sont les organismes photosynthétiques les plus abondants dans notre environnement, elles assurent environ 30 à 40% de la production d'O2, et de la consommation du CO2 par les océans et constituent le premier maillon de la chaîne alimentaire. A part la photosynthèse, leur métabolisme est encore très mal connu. Ainsi, pour mieux comprendre le métabolisme cyanobactérien et proposer des stratégies de reprogrammation, il est primordial de développer des méthodes analytiques permettant l’étude globale de leur métabolisme en réponse à des variations de conditions environnementales et de stress. La cyanobactérie modèle Synechocystis PCC6803 convient parfaitement à ce type d’analyse. En effet, Synechocystis est un unicellulaire, hétérotrophe facultative capable de se développer en eau douce ou saumâtre et à un pH alcalin. Synechocystis possède un petit génome d’environ 4.0 Mb entièrement séquencé et facilement manipulable grâce aux outils développés au laboratoire. Son génome prédit l'existence d'un métabolisme carboné complexe mais encore peu étudié. Mon travail de thèse est centré sur cette analyse par la combinaison de deux approches, la génomique fonctionnelle et la métabolomique. Durant ma thèse en collaboration avec le LEMM dirigé par Christophe Junot iBiTec-S/SPI, j’ai développé un protocole d’extraction des métabolites de Synechocystis, ainsi qu’une méthode d’analyse métabolomique par couplage de la chromatographie liquide à la spectrométrie de masse LTQ-Orbitrap à haute résolution. L’application de cette nouvelle méthode analytique m’a permis d’étudier l’influence de la lumière et du glucose sur le métabolisme de Synechocystis. Ainsi, j’ai montré que Synechocystis cultivée en présence du glucose reprogramme fortement son métabolisme. Parmi les résultats très intéressants, j’ai montré que le glucose engendre un stress oxydant. Chez tous les organismes, une forte activité du métabolisme carboné entraîne la production de métabolites toxiques tels que le méthyglyoxal (MG). Le MG modifie irréversiblement de nombreuses bio-molécules. Dans le cadre de ma thèse, j’ai commencé à m’intéresser à l'effet du MG sur la physiologie et le métabolisme de Synechocystis. J'ai construit 25 mutants KO pour les gènes de la glycolyse et du métabolisme du glycérol permettant de moduler la concentration intracellulaire de MG et également les gènes impliqués dans les voies de détoxication du MG dont celle dépendante de la synthèse du GSH (la voie des glyoxalases). J’ai pu montrer que les gènes responsables de la synthèse du GSH sont essentiels à la viabilité cellulaire. Je suis parvenu toutefois à obtenir un mutant déplété de gshB et ne produisant plus de GSH à un niveau détectable. En faisant une analyse métabolomique approfondie, j’ai mis en évidence pour la première fois que Synechocystis était capable produire deux tripeptides non-thiolés analogues structuraux du GSH;… Advisors/Committee Members: Cassier-Chauvat, Corinne (thesis director).

Subjects/Keywords: Cyanobactérie; Synechocystis; Métabolomique; Méthylglyoxal; Glutathion; Glyoxalases; Glutathion synthase; Glutathion synthétase; GammaGlutamylcystéine; Cyanobacterium; Synechocystis; Central carbon metabolism; Methylglyxa; Metabolic reprogramming; Glyoxalases; Glutathione; Glutathion synthétase; GammaGlutamylcystéine

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Narainsamy, K. (2012). Biologie systémique de la résistance au stress oxydant métabolique : rôles du glutathion, du méthylglyoxal et des glyoxalases : System biology of the metabolic oxydative stress resistance : role of glutathione, methylglyoxal and glyoxalases. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2012PA112099

Chicago Manual of Style (16^th Edition):

Narainsamy, Kinsley. “Biologie systémique de la résistance au stress oxydant métabolique : rôles du glutathion, du méthylglyoxal et des glyoxalases : System biology of the metabolic oxydative stress resistance : role of glutathione, methylglyoxal and glyoxalases.” 2012. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed January 22, 2021. http://www.theses.fr/2012PA112099.

MLA Handbook (7^th Edition):

Narainsamy, Kinsley. “Biologie systémique de la résistance au stress oxydant métabolique : rôles du glutathion, du méthylglyoxal et des glyoxalases : System biology of the metabolic oxydative stress resistance : role of glutathione, methylglyoxal and glyoxalases.” 2012. Web. 22 Jan 2021.

Vancouver:

Narainsamy K. Biologie systémique de la résistance au stress oxydant métabolique : rôles du glutathion, du méthylglyoxal et des glyoxalases : System biology of the metabolic oxydative stress resistance : role of glutathione, methylglyoxal and glyoxalases. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2012. [cited 2021 Jan 22]. Available from: http://www.theses.fr/2012PA112099.

Council of Science Editors:

Narainsamy K. Biologie systémique de la résistance au stress oxydant métabolique : rôles du glutathion, du méthylglyoxal et des glyoxalases : System biology of the metabolic oxydative stress resistance : role of glutathione, methylglyoxal and glyoxalases. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2012. Available from: http://www.theses.fr/2012PA112099

Michigan State University

22. Brady, Paul Scott. The relationship of the glutathione peroxidase system to physical stress.

Degree: PhD, 1978, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:28689

Subjects/Keywords: Glutathione – Metabolism; Selenium – Physiological effect; Vitamin E deficiency; Exercise – Physiological aspects

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APA (6^th Edition):

Brady, P. S. (1978). The relationship of the glutathione peroxidase system to physical stress. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:28689

Chicago Manual of Style (16^th Edition):

Brady, Paul Scott. “The relationship of the glutathione peroxidase system to physical stress.” 1978. Doctoral Dissertation, Michigan State University. Accessed January 22, 2021. http://etd.lib.msu.edu/islandora/object/etd:28689.

MLA Handbook (7^th Edition):

Brady, Paul Scott. “The relationship of the glutathione peroxidase system to physical stress.” 1978. Web. 22 Jan 2021.

Vancouver:

Brady PS. The relationship of the glutathione peroxidase system to physical stress. [Internet] [Doctoral dissertation]. Michigan State University; 1978. [cited 2021 Jan 22]. Available from: http://etd.lib.msu.edu/islandora/object/etd:28689.

Council of Science Editors:

Brady PS. The relationship of the glutathione peroxidase system to physical stress. [Doctoral Dissertation]. Michigan State University; 1978. Available from: http://etd.lib.msu.edu/islandora/object/etd:28689

Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

23. Σταυρινού, Παντελής. Μελέτη της έκφρασης των ενζύμων και ομάδας γονιδίων που εμπλέκονται στο μεταβολισμό φαρμάκων και ξενοβιοτικών ουσιών σε όγκους εγκεφάλου.

Degree: 2011, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ)

URL: http://hdl.handle.net/10442/hedi/33159

►

We set out to study the expression profile of various genes and their respective proteins that are related to drug metabolism in human brain tumors.… (more)

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We set out to study the expression profile of various genes and their respective proteins that are related to drug metabolism in human brain tumors. Brain tumor samples were collected only from newly diagnosed patients that hadn’t undergone previous radiation or chemotherapy. Using western blotting and quantitative real time PCR the protein and mRNA expression of aldehyde oxidase-1 (AOX1), glutathione-S-transferase (GSTs) -P, -T, M and cytochrome P450 1A1 (CYP1A1) were assessed. The gene expression profile of aldehyde dehydrogenase 3A1 (ALDH3A1) and cytochrome P450 1B1 (CYP1B1) were also evaluated. A total of 77 specimens were analyzed. We determined the expression of five proteins (CYP1A1, AOX1, GSTP, GSTT, and GSTM) in 54 surgical samples. We compared for any significant difference in the mean protein expression between meningiomas and astrocytomas. On average meningiomas expressed higher AOX1, GSTP and GSTM levels than astrocytomas (AOX: p=0,03, GSTP: p=0,009 and GSTM: p<0,001) but lower CYP1A1 levels (p=0,01). Correlation between the four degrees of malignancy (WHO I-IV) and the protein expression levels was evaluated. A significant negative correlation between malignancy grade and protein levels for AOX, GSTP and GSTM (p=0,002, p=0,004 and p=0,006 respectively) was reported. We also examined for any differences among the levels of the transcript product in a total of 47 tissue specimens. There were 20 meningiomas, 15 astrocytomas and 5 metastases. mRNA levels of CYP1B1, AOX1, GSTP1 and GSTM3 were significantly affected by the underlying pathology (p<0,05). Meningiomas had consistently higher mRNA levels than astrocytomas for the four abovementioned genes (UCYP1B1=33,5, p<0,001, UAOX1=14, p<0,001, UGSTP1=34, p<0,001 and UGSTM3=76,5, p=0,013). When comparing meningiomas with the metastasis group, the two genes that demonstrated the highest mRNA levels, namely AOX1 (M=12,81) and GSTM3 (M=7,89) retained their statistical significance in the difference between the two groups (UAOX1=5, p=0,001 and UGSTM3=8, p=0,002respectively). Lastly, the comparison among astrocytomas and adenocarcinomas only revealed a significant difference for the GSTP1 gene (UGSTP1=8, p=0,007). There was a significant negative correlation between malignancy grade and mRNA levels for AOX, GSTP1, GSTM3 and also for CYP1B1 (p=0,002, p=0,001, p=0,006 and p<0,001 respectively). For 32 samples, we were able to run both western and RT-PCR analysis. There is absolutely no correlation for any of the studied genes for the meningiomas group while there is one for AOX1 (p=0,011), GSTP1 (p=0,03), GSTM3 (p=0,02) in the astrocytomas group. We showed that the various CNS tumors show different patterns of drug metabolizing enzyme (DME) expression. Meningiomas exhibited significantly higher expression levels for the DMEs studied. For AOX1, GSTP and GSTM, this was shown on both a transcriptional and a translational level. For astrocytomas, we observed a correlation between mRNA levels and the translational product.

Ο σκοπός της παρούσης εργασίας είναι η μελέτη…

Subjects/Keywords: S-τρανσφεράσες της γλουταθειόνης; Αλδεϋδική δεϋδρογενάση; Αλδεϋδική οξειδάση; Ένζυμα κυτοχρώματος P450; Όγκοι εγκεφάλου; Μεταβολισμός; Χημειοθεραπεία; Φάρμακα; Glutathione-S-transferase; ALDEHYDE DEHYDROGENASE; Aldehyde oxidase; Cytochrome P450; Brain tumors; Metabolism; Chemotherapy; Drugs

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Σταυρινού, . �. (2011). Μελέτη της έκφρασης των ενζύμων και ομάδας γονιδίων που εμπλέκονται στο μεταβολισμό φαρμάκων και ξενοβιοτικών ουσιών σε όγκους εγκεφάλου. (Thesis). Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/33159

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Σταυρινού, Παντελής. “Μελέτη της έκφρασης των ενζύμων και ομάδας γονιδίων που εμπλέκονται στο μεταβολισμό φαρμάκων και ξενοβιοτικών ουσιών σε όγκους εγκεφάλου.” 2011. Thesis, Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ). Accessed January 22, 2021. http://hdl.handle.net/10442/hedi/33159.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Σταυρινού, Παντελής. “Μελέτη της έκφρασης των ενζύμων και ομάδας γονιδίων που εμπλέκονται στο μεταβολισμό φαρμάκων και ξενοβιοτικών ουσιών σε όγκους εγκεφάλου.” 2011. Web. 22 Jan 2021.

Vancouver:

Σταυρινού �. Μελέτη της έκφρασης των ενζύμων και ομάδας γονιδίων που εμπλέκονται στο μεταβολισμό φαρμάκων και ξενοβιοτικών ουσιών σε όγκους εγκεφάλου. [Internet] [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2011. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10442/hedi/33159.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Σταυρινού �. Μελέτη της έκφρασης των ενζύμων και ομάδας γονιδίων που εμπλέκονται στο μεταβολισμό φαρμάκων και ξενοβιοτικών ουσιών σε όγκους εγκεφάλου. [Thesis]. Aristotle University Of Thessaloniki (AUTH); Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (ΑΠΘ); 2011. Available from: http://hdl.handle.net/10442/hedi/33159

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Missouri – Columbia

24. Patton, John David, 1976-. GABP regulation of the murine GABPa/ATPsynthase coupling factor six and human glutathione reductase promoters.

Degree: PhD, 2005, University of Missouri – Columbia

URL: http://hdl.handle.net/10355/4122

► GABPa is expressed from a bi-directional promoter expressing ATP synthase coupling factor six (CF6) in the opposite direction. This bi-directional promoter is regulated by GABP,… (more)

Subjects/Keywords: GA-Binding Protein Transcription Factor – metabolism; Glutathione Reductase – genetics; Glutathione Reductase – biosynthesis; GA-Binding Protein Transcription Factor – genetics; Mitochondrial Proton-Translocating ATPases – genetics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Patton, John David, 1. (2005). GABP regulation of the murine GABPa/ATPsynthase coupling factor six and human glutathione reductase promoters. (Doctoral Dissertation). University of Missouri – Columbia. Retrieved from http://hdl.handle.net/10355/4122

Chicago Manual of Style (16^th Edition):

Patton, John David, 1976-. “GABP regulation of the murine GABPa/ATPsynthase coupling factor six and human glutathione reductase promoters.” 2005. Doctoral Dissertation, University of Missouri – Columbia. Accessed January 22, 2021. http://hdl.handle.net/10355/4122.

MLA Handbook (7^th Edition):

Patton, John David, 1976-. “GABP regulation of the murine GABPa/ATPsynthase coupling factor six and human glutathione reductase promoters.” 2005. Web. 22 Jan 2021.

Vancouver:

Patton, John David 1. GABP regulation of the murine GABPa/ATPsynthase coupling factor six and human glutathione reductase promoters. [Internet] [Doctoral dissertation]. University of Missouri – Columbia; 2005. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10355/4122.

Council of Science Editors:

Patton, John David 1. GABP regulation of the murine GABPa/ATPsynthase coupling factor six and human glutathione reductase promoters. [Doctoral Dissertation]. University of Missouri – Columbia; 2005. Available from: http://hdl.handle.net/10355/4122

25. Σέγκος, Δημήτριος. Μελέτη ηπατικών βλαβών και μεταβολών στο σύστημα του κυτοχρώματος P-450 κατά την χορήγηση παρακεταμόλης και φαινοβαρβιτάλης σε επίμυς υπό δίαιτα χαμηλής περιεκτικότητας σε χολίνη.

Degree: 2007, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/24541

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Aim of the study. The aim of the study was to examine the counteraction between choline deficient diet (CDD) and paracetamole (ACET) or phenobarbital (PB)… (more)

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Aim of the study. The aim of the study was to examine the counteraction between choline deficient diet (CDD) and paracetamole (ACET) or phenobarbital (PB) administration. Methods. A toxic dose of paracetamole or an inductive dose of phenobarbital was administered to male Wistar rats under CDD. The following were studied: a) body weight, b) AST, ALT ALP, c) liver histologic examination, d) liver GSH content liver GST activity, e) liver P450 IA1 P450 IA2 Ρ450 IIΕ1 Ρ450 IIΒ1/2 activity and protein level. Results. Paracetamole administration was followed by: 1) an increase of AST and ALT in both CDD and normal diet (ND) rats and a decrease of ALP in CDD rats only, 2) inflammatory response centrilobular necrosis and mitotic activity increase in both CDD and ND rats, 3) a decrease of GSH content in ND rats and an increase of GSH content in CDD rats, 4) an increase of CYPIA2 both protein level and activity in ND rats and a decrease of CYPIA2 both protein level and activity in CDD rats an increase of CYPIIE1 protein level in both CDD and ND rats but no effect on CYPEIIE1 activity in both CDD and ND rats a decrease of CYPIIB1/2 both protein level and activity in CDD rats, and an increase of CYPIIB1/2 protein level in ND rats but no effect on CYPIIB1/2 activity in ND rats. Phenobarbital administration was followed by: 1) an increase of AST in CDD rats only, 2) necrosis of low severity in both CDD and ND rats; a mitotic activity increase in ND rats only 3) an increase of GST activity in CDD rats only, 4) an increase of the activity of CYPIA1 CYPIA2 CYPIIE1 and CYPIIB1/2 under both diets; an increase of the protein level of CYPIA1 and CYPIIB 1/2 under both diets; a decrease of CYPIA2 protein level in CDD rats only; a decrease of CYPIIE1 protein level in CDD and ND rats. Conclusions. CDD altered the toxic and inductive effects of ACET and PB in the liver.

Σκοπός της διατριβής. Μελέτη της αλληλεπίδρασης της διαιτητικής έλλειψης χολίνης (CDD) μετά από χορήγηση παρακεταμόλης η φαινοβαρβιτάλης. Πειραματόζωα και μέθοδος. Τοξική δόση παρακεταμόλης (ACET) η χαμηλή επαγωγική δόση φαινοβαρβιτάλης (PB) χορηγήθηκε σε άρρενες επίμυς τύπου Wistar υπό CDD. Προσδιορίσθηκαν: α) βάρος σώματος, β) AST ALT ALP ορού, γ) ιστολογική εξέταση ήπατος, δ) ποσόν GSH ήπατος και δραστικότητα GST ήπατος, ε) έκφραση των CYPIA1 CYPIA2 CYPEIIE1 CYPIIB1/2 στο ήπαρ. Αποτελέσματα. Διαπιστώθηκαν οι έξης μεταβολές ACET: 1) αύξηση της AST και της ALT σε επίμυς υπό CDD η φυσιολογική δίαιτα (ΦΔ) και μείωση της ALP μόνον σε επίμυς υπό CDD, 2) φλεγμονώδης αντίδραση κεντρολοβιακή νέκρωση και αύξηση της μιτωτικής δραστηριότητας σε επίμυς υπό CDD η ΦΔ, 3) μείωση GSH σε επίμυς υπό ΦΔ και αύξηση της σε επίμυς υπό CDD, 4) αύξηση της έκφρασης του CYPIA2 υπό ΦΔ και μείωση της υπό CDD, 5) αύξηση του ποσού CYPIIE1 υπό CDD η ΦΔ, 6) μείωση της έκφρασης του CYPIIB1/2 υπό CDD άλλα αύξηση του ποσού του CYPIIB1/2 χωρίς μεταβολή της δραστικότητας του υπό ΦΔ. PB: 1) αύξηση της AST μόνον υπό CDD, 2) νέκρωση μικρής βαρύτητας σε επίμυς υπό CDD η ΦΔ και αύξηση της μιτωτικής δραστηριότητος…

Subjects/Keywords: Δίαιτα; Χολίνη; Μεταβολισμός; Παρακεταμόλη; Φαινοβαρβιτάλη; Γλουταθειόνη; Επίμυες; Diet; Choline; Metabolism; Paracetamole; Phenobarbital; P-450; Glutathione; Rats

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APA (6^th Edition):

Σέγκος, . �. (2007). Μελέτη ηπατικών βλαβών και μεταβολών στο σύστημα του κυτοχρώματος P-450 κατά την χορήγηση παρακεταμόλης και φαινοβαρβιτάλης σε επίμυς υπό δίαιτα χαμηλής περιεκτικότητας σε χολίνη. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/24541

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Σέγκος, Δημήτριος. “Μελέτη ηπατικών βλαβών και μεταβολών στο σύστημα του κυτοχρώματος P-450 κατά την χορήγηση παρακεταμόλης και φαινοβαρβιτάλης σε επίμυς υπό δίαιτα χαμηλής περιεκτικότητας σε χολίνη.” 2007. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 22, 2021. http://hdl.handle.net/10442/hedi/24541.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Σέγκος, Δημήτριος. “Μελέτη ηπατικών βλαβών και μεταβολών στο σύστημα του κυτοχρώματος P-450 κατά την χορήγηση παρακεταμόλης και φαινοβαρβιτάλης σε επίμυς υπό δίαιτα χαμηλής περιεκτικότητας σε χολίνη.” 2007. Web. 22 Jan 2021.

Vancouver:

Σέγκος �. Μελέτη ηπατικών βλαβών και μεταβολών στο σύστημα του κυτοχρώματος P-450 κατά την χορήγηση παρακεταμόλης και φαινοβαρβιτάλης σε επίμυς υπό δίαιτα χαμηλής περιεκτικότητας σε χολίνη. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2007. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10442/hedi/24541.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Σέγκος �. Μελέτη ηπατικών βλαβών και μεταβολών στο σύστημα του κυτοχρώματος P-450 κατά την χορήγηση παρακεταμόλης και φαινοβαρβιτάλης σε επίμυς υπό δίαιτα χαμηλής περιεκτικότητας σε χολίνη. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2007. Available from: http://hdl.handle.net/10442/hedi/24541

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

26. Peris Franquet, Eduard. Adipose tissue mitchondrial function is modulated by antioxidants.

Degree: 2019, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/60772

► Antioxidants are widely used as reactive oxygen species (ROS) scavenging agents in experimental research and in conditions where oxidative stress plays a primary role. However,… (more)

▼ Antioxidants are widely used as reactive oxygen species (ROS) scavenging agents in experimental research and in conditions where oxidative stress plays a primary role. However, the effect of antioxidant supplementation on white and brown adipose tissue functionality is understudied, and the role of ROS and/or antioxidant treatment during adipose tissue browning, a process in which the adipocytes’ mitochondrial density and activity increase, is largely unknown. In paper I, by using antioxidants and ROS-sensitive fluorescent probes in cultured β3-AR-stimulated adipocytes, we observed that 24-48-hour antioxidant treatment increases the mitochondrial ROS production associated with reduced respiration and increased glycolysis. Moreover, treatment of mice with the antioxidant N-acetylcysteine (NAC) blunted the β3-AR agonist-induced browning response of white adipose tissue and reduced the mitochondrial activity in brown adipose tissue even in the absence of β3-AR stimulation. Previous studies have shown positive effects of prolonged NAC treatment on whole-body metabolism in mice. In light of these seemingly contradictory results, we hypothesize that chronic antioxidant exposure, in a dose-dependent manner, can lead to so-called mitohormesis. Indeed, in paper II, by treating mice with a set of different NAC doses across a defined time course, we found that prolonged supplementation with a high dose of NAC leads to increased mitochondrial function of white adipose tissue, reduced fat mass and improved insulin sensitivity. In summary, this thesis demonstrates that the adipose tissue response to antioxidant treatment in mice is biphasic and tightly connected to the adipose tissue type, the dosage and the treatment duration. This thesis also provides an alternative explanation for previously reported controversial findings where antioxidants (such as NAC) have exerted deleterious effects on health. Finally, the results of this thesis provide new insights into the appropriate design of antioxidant treatment studies: optimizing treatment dosage and duration may be the key to achieve success with antioxidant therapy.Based on previous research, we hypothesized that reactive oxygen species (ROS)/redox signaling plays a role in β3-AR agonist-induced browning. To test this hypothesis, we analyzed the effect of antioxidant treatment on β3-AR agonist-induced browning in cultured adipocytes. Using ROS-sensitive fluorescent probes to measure changes in total and mitochondrial ROS production in combination with Seahorse technology-based oxygen consumption measurements, we made the surprising observation that antioxidant treatment has a negative impact on adipocyte mitochondrial function even in absence of β3-AR-stimulation. This effect associated with increased mitochondrial ROS production. While similar pro-oxidant effects of antioxidants - sometimes referred to as reductive stress, where electrons are donated to oxygen leading to increased ROS-production - have been reported in a few other studies, it’s an understudied and, in our…

Subjects/Keywords: adipocyte; metabolism; browning; antioxidant; mitochondria; oxidative stress; adrenergic recpetor; N-acetylcysteine; glutathione; reactive oxygen species

…Weight and Food Intake and Increases Thermogenesis to Regulate Energy Metabolism. Cell Reports… …Glucose transporter type 4 Reduced glutathione Oxidized glutathione Gonadal white adipose tissue… …leptin and adiponectin contribute to the regulation of whole-body energy balance and metabolism… …metabolism even in adulthood (Cypess, Lehman et al. 2009). In rodents, BAT is mainly… …metabolism across their whole life. Interestingly, fate-mapping studies combined with cell sorting…

10 more images…

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APA (6^th Edition):

Peris Franquet, E. (2019). Adipose tissue mitchondrial function is modulated by antioxidants. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/60772

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Peris Franquet, Eduard. “Adipose tissue mitchondrial function is modulated by antioxidants.” 2019. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 22, 2021. http://hdl.handle.net/2077/60772.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Peris Franquet, Eduard. “Adipose tissue mitchondrial function is modulated by antioxidants.” 2019. Web. 22 Jan 2021.

Vancouver:

Peris Franquet E. Adipose tissue mitchondrial function is modulated by antioxidants. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2019. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2077/60772.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Peris Franquet E. Adipose tissue mitchondrial function is modulated by antioxidants. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2019. Available from: http://hdl.handle.net/2077/60772

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université de Lorraine

27. Lallement, Pierre-Alexandre. Caractérisation biochimique et fonctionnelle de glutathion transférases à cystéine catalytique de peuplier (Populus trichocarpa) : Biochemical and functional characterization of poplar glutathione S-transferases containing a cysteine as a catalytic residue.

Degree: Docteur es, Biologie végétale et forestière, 2014, Université de Lorraine

URL: http://www.theses.fr/2014LORR0275

►

Les glutathion transférases (GSTs) constituent une superfamille ubiquitaire d’enzymes multifonctionnelles impliquées dans les processus de détoxication cellulaire en métabolisant des substrats exogènes appelés xénobiotiques et… (more)

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Les glutathion transférases (GSTs) constituent une superfamille ubiquitaire d’enzymes multifonctionnelles impliquées dans les processus de détoxication cellulaire en métabolisant des substrats exogènes appelés xénobiotiques et dans le métabolisme secondaire. Pour cela, ces enzymes peuvent catalyser la conjugaison d’une molécule de glutathion (GSH) sur les composés ciblés ou simplement les lier au travers d’une fonction ligandine. Alors que la fonction de conjugaison est catalysée par les GSTs possédant une sérine ou une tyrosine comme résidu catalytique, certaines d’entre elles possèdent à la place une cystéine. Cette substitution change radicalement leurs propriétés puisque les GSTs à cystéine (Cys-GSTs) catalysent plutôt des réactions de déglutathionylation. Les Cys-GSTs sont retrouvées chez la plupart des organismes et sont réparties en plusieurs classes. Chez les plantes, on trouve principalement 4 classes : déshydroascorbate réductases (DHARs), GSTs Lambda (GSTLs), glutathionyl hydroquinone réductases (GHRs) et mPGES2 (microsomal prostaglandine E-synthase type 2). Alors que le rôle des DHARs semble clairement associé à la réduction du déshydroascorbate en ascorbate, la fonction physiologique des autres Cys-GSTs reste majoritairement inconnue. En combinant des approches moléculaires, cellulaires, biochimiques et structurales, l’analyse fonctionnelle des deux GHRs, des trois GSTLs et des trois DHARs chez l’arbre modèle Populus trichocarpa a été entreprise. De façon intéressante, les gènes GSTL et GHR sont majoritairement exprimés dans les fleurs, les fruits et les pétioles par rapport aux feuilles et aux racines. A l’inverse, les gènes DHAR sont principalement exprimés dans les feuilles. De plus, l’expression transitoire de protéines fusionnées à la GFP dans le tabac a montré que les GSTLs et les DHARs sont localisées dans les plastes, le cytoplasme et le noyau alors que les GHRs sont toutes plastidiales. Les études biochimiques et structurales effectuées à l’aide des protéines recombinantes et de substrats modèles ont montré que la plupart des Cys-GSTs possèdent des activités et des structures assez semblables. Cependant, bien que les GSTLs et les DHARs adoptent un repliement GST canonique classique proche de celui des GSTs Oméga fongiques et humaines, elles sont monomériques alors que les GSTs Oméga sont dimériques. Les GHRs sont particulières tant au niveau de leur interface de dimérisation unique qu’au niveau de leurs propriétés spécifiques de réduction de quinones glutathionylées. En résumé, la nature des substrats fixés par les Cys-GSTs (composés cycliques aromatiques) ainsi que les territoires d’expression de ces gènes et protéines suggèrent que ces protéines sont globalement impliquées dans la protection des plantes face aux contraintes environnementales via la modification, le stockage et/ou le transport de métabolites secondaires et autres composés antioxydants. Toutefois, l’objectif suivant sera de déterminer la nature exacte des substrats/ligands associés à chaque enzyme

Glutathione transferases…

Advisors/Committee Members: Rouhier, Nicolas (thesis director), Hecker, Arnaud (thesis director).

Subjects/Keywords: Glutathion transférases; Cystéine catalytique; Populus trichocarpa; Déglutathionylation; Structures cristallographiques; Détoxication; Espèces oxygénées réactives; Métabolisme secondaire; Glutathione transferases; Catalytic cysteine; Populus trichocarpa; Deglutathionylation; Crystal structures; Detoxification; Reactive oxygen species; Secondary metabolism; 572.792

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lallement, P. (2014). Caractérisation biochimique et fonctionnelle de glutathion transférases à cystéine catalytique de peuplier (Populus trichocarpa) : Biochemical and functional characterization of poplar glutathione S-transferases containing a cysteine as a catalytic residue. (Doctoral Dissertation). Université de Lorraine. Retrieved from http://www.theses.fr/2014LORR0275

Chicago Manual of Style (16^th Edition):

Lallement, Pierre-Alexandre. “Caractérisation biochimique et fonctionnelle de glutathion transférases à cystéine catalytique de peuplier (Populus trichocarpa) : Biochemical and functional characterization of poplar glutathione S-transferases containing a cysteine as a catalytic residue.” 2014. Doctoral Dissertation, Université de Lorraine. Accessed January 22, 2021. http://www.theses.fr/2014LORR0275.

MLA Handbook (7^th Edition):

Lallement, Pierre-Alexandre. “Caractérisation biochimique et fonctionnelle de glutathion transférases à cystéine catalytique de peuplier (Populus trichocarpa) : Biochemical and functional characterization of poplar glutathione S-transferases containing a cysteine as a catalytic residue.” 2014. Web. 22 Jan 2021.

Vancouver:

Lallement P. Caractérisation biochimique et fonctionnelle de glutathion transférases à cystéine catalytique de peuplier (Populus trichocarpa) : Biochemical and functional characterization of poplar glutathione S-transferases containing a cysteine as a catalytic residue. [Internet] [Doctoral dissertation]. Université de Lorraine; 2014. [cited 2021 Jan 22]. Available from: http://www.theses.fr/2014LORR0275.

Council of Science Editors:

Lallement P. Caractérisation biochimique et fonctionnelle de glutathion transférases à cystéine catalytique de peuplier (Populus trichocarpa) : Biochemical and functional characterization of poplar glutathione S-transferases containing a cysteine as a catalytic residue. [Doctoral Dissertation]. Université de Lorraine; 2014. Available from: http://www.theses.fr/2014LORR0275

University of Gothenburg / Göteborgs Universitet

28. Andresen Bergström, Moa 1978-. Bioactivation of Xenobiotics in the Skin. Mechanistic Investigations and Structure-Activity Relationship Studies of Alkene and Oxime Prohaptens in Contact Allergy.

Degree: 2007, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/17143

Subjects/Keywords: Allergic contact dermatitis; Bionucleophile; Cytochrome P450; Dendritic cell; Epoxide; FCAT; Glutathione; LLNA; Metabolism; Metabolic activation; Nitroso; Prohapten; Sensitisation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Andresen Bergström, M. 1. (2007). Bioactivation of Xenobiotics in the Skin. Mechanistic Investigations and Structure-Activity Relationship Studies of Alkene and Oxime Prohaptens in Contact Allergy. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/17143

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Andresen Bergström, Moa 1978-. “Bioactivation of Xenobiotics in the Skin. Mechanistic Investigations and Structure-Activity Relationship Studies of Alkene and Oxime Prohaptens in Contact Allergy.” 2007. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 22, 2021. http://hdl.handle.net/2077/17143.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Andresen Bergström, Moa 1978-. “Bioactivation of Xenobiotics in the Skin. Mechanistic Investigations and Structure-Activity Relationship Studies of Alkene and Oxime Prohaptens in Contact Allergy.” 2007. Web. 22 Jan 2021.

Vancouver:

Andresen Bergström M1. Bioactivation of Xenobiotics in the Skin. Mechanistic Investigations and Structure-Activity Relationship Studies of Alkene and Oxime Prohaptens in Contact Allergy. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2007. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2077/17143.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Andresen Bergström M1. Bioactivation of Xenobiotics in the Skin. Mechanistic Investigations and Structure-Activity Relationship Studies of Alkene and Oxime Prohaptens in Contact Allergy. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2007. Available from: http://hdl.handle.net/2077/17143

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Carolina – Greensboro

29. Fordahl, Steven C. Effects of manganese exposure and antioxidant therapy on oxidative stress and stereotypic behaviors in rats.

Degree: 2009, University of North Carolina – Greensboro

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2488

► Manganese (Mn) is an essential dietary element required for several important physiological processes. However, accumulation of Mn due to excessive environmental exposure is known to… (more)

▼ Manganese (Mn) is an essential dietary element required for several important physiological processes. However, accumulation of Mn due to excessive environmental exposure is known to pose neurological health concerns that manifest as movement abnormalities and cognitive impairment. Oxidative stress has been hypothesized to play a role in this dysfunction. In these studies we examined the effect Mn exposure had on oxidative stress in the brain with or without antioxidant therapy, and how brain regional Mn accumulation affected stereotypic behaviors in rats. Sprague-Dawley rats raised on AIN-93G diet were randomized into a Mn free group (deionized water) and Mn exposed group (deionized water with 1 g Mn/L). Each group was then subdivided into three additional groups receiving injections of either saline (vehicle) or antioxidant therapy: 200 mg/kg N-acetyl-cysteine (NAC) or 5 mg/kg (-)-epigallocatechin-3-gallate (EGCG) to yield six groups total, each with an n=6. During the sixth week of treatment, stereotypic rat behaviors (total distance traveled, sleep, sniff, and groom) were monitored using Clever Systems Home Cage Scan. Upon completion of the sixth week the rat brains were removed with the caudate putamen (CP) and hippocampus (HC) sectioned out and analyzed for Mn and iron (Fe) concentrations, total glutathione (GSH) levels, lipid peroxidation in the form of F2-Isoprostanes (F2-IsoPs), along with glutathione peroxidase (GPx) and catalase mRNA levels. Results were considered significant when p≤0.05. Mn exposure significantly increased Mn concentrations in both the CP and HC, accompanied by significantly decreased Fe:Mn ratios in Mn-exposed groups. Mn significantly increased total distance traveled in each Mn-exposed group and decreased sniff behavior in the Mn only group. Only modest alterations in GSH and catalase levels were present in each region, although, a significant positive correlation between Mn concentration and GPx mRNA expression was observed. Additionally, F2-IsoP results showed no evidence of increased oxidative damage compared to CN regardless of EGCG or NAC therapy. These data, compared to the body of Mn toxicity research, suggest that oral Mn exposure may not generate deleterious levels of oxidative stress leading to overt neurological dysfunction. This exposure paradigm, instead, may result in subtle neurochemical alterations associated with behavior change and potential cognitive impairment.; Behavior, EGCG, Glutathione, Manganese, Neurotoxicity, Oxidative Stress Advisors/Committee Members: Keith Erikcon (advisor).

Subjects/Keywords: Manganese – Metabolism.; Oxidative stress.; Manganese – Toxicology.; Neurotoxic agents.; Cognition disorders.; Glutathione.; Rats – Behavior – Research.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fordahl, S. C. (2009). Effects of manganese exposure and antioxidant therapy on oxidative stress and stereotypic behaviors in rats. (Masters Thesis). University of North Carolina – Greensboro. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2488

Chicago Manual of Style (16^th Edition):

Fordahl, Steven C. “Effects of manganese exposure and antioxidant therapy on oxidative stress and stereotypic behaviors in rats.” 2009. Masters Thesis, University of North Carolina – Greensboro. Accessed January 22, 2021. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2488.

MLA Handbook (7^th Edition):

Fordahl, Steven C. “Effects of manganese exposure and antioxidant therapy on oxidative stress and stereotypic behaviors in rats.” 2009. Web. 22 Jan 2021.

Vancouver:

Fordahl SC. Effects of manganese exposure and antioxidant therapy on oxidative stress and stereotypic behaviors in rats. [Internet] [Masters thesis]. University of North Carolina – Greensboro; 2009. [cited 2021 Jan 22]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2488.

Council of Science Editors:

Fordahl SC. Effects of manganese exposure and antioxidant therapy on oxidative stress and stereotypic behaviors in rats. [Masters Thesis]. University of North Carolina – Greensboro; 2009. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=2488

Portland State University

30. Shaw, Collin M. Increased Glutathione Metabolic Defense Capabilities in Cultured Alzheimer's Diseased Lymphoblast Cell Lines.

Degree: MS(M.S.) in Biology, Biology, 1998, Portland State University

URL: https://pdxscholar.library.pdx.edu/open_access_etds/1703

► The hypothesis to be tested states that the pathology of Alzheimer's disease (AD) involves elevated levels of oxidative stress, resulting in elevated levels of… (more)

Subjects/Keywords: Alzheimer's disease – Pathophysiology; Glutathione – Metabolism; Lymphocytes; Oxidative stress; Nervous system – Degeneration; Nervous System Diseases; Other Cell and Developmental Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Shaw, C. M. (1998). Increased Glutathione Metabolic Defense Capabilities in Cultured Alzheimer's Diseased Lymphoblast Cell Lines. (Masters Thesis). Portland State University. Retrieved from https://pdxscholar.library.pdx.edu/open_access_etds/1703

Chicago Manual of Style (16^th Edition):

Shaw, Collin M. “Increased Glutathione Metabolic Defense Capabilities in Cultured Alzheimer's Diseased Lymphoblast Cell Lines.” 1998. Masters Thesis, Portland State University. Accessed January 22, 2021. https://pdxscholar.library.pdx.edu/open_access_etds/1703.

MLA Handbook (7^th Edition):

Shaw, Collin M. “Increased Glutathione Metabolic Defense Capabilities in Cultured Alzheimer's Diseased Lymphoblast Cell Lines.” 1998. Web. 22 Jan 2021.

Vancouver:

Shaw CM. Increased Glutathione Metabolic Defense Capabilities in Cultured Alzheimer's Diseased Lymphoblast Cell Lines. [Internet] [Masters thesis]. Portland State University; 1998. [cited 2021 Jan 22]. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/1703.

Council of Science Editors:

Shaw CM. Increased Glutathione Metabolic Defense Capabilities in Cultured Alzheimer's Diseased Lymphoblast Cell Lines. [Masters Thesis]. Portland State University; 1998. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/1703

Open Access Theses and Dissertations