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You searched for subject:(oxidant therapy). Showing records 1 – 3 of 3 total matches.

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University of Florida

1. Dutta, Debapriya. The Role of Autophagy in Oxidative Stress-Mediated Dysfunction in Cardiac Cells and Rodent Hearts.

Degree: PhD, Medical Sciences - Molecular Cell Biology (IDP), 2012, University of Florida

Cardiovascular disease (CVD) is the leading cause ofmortality and morbidity in the developing world. While long-term exposure to cardiovascular risk factors plays a majorrole in the etiopathogenesis of CVD, oxidative stress-induced cardiac damage enhances the susceptibility to developheart pathologies in late life. The enhanced generation of reactive oxygenspecies, especially by damaged mitochondria, is considered to be a majorcontributing mechanism. Hence, the removal of oxidatively modified cellularcomponents and dysfunctional mitochondria is critical for maintenance of cellularhomeostasis. Autophagy isa self-digestion process which can degrade damaged proteins and organelles andis also the only known mechanism targeting dysfunctional mitochondria for removal.In our studies, we have investigated whether pharmacological ornutritional enhancement of autophagy offers protection against oxidativestress-mediated dysfunction in a cardiomyocyte cell line (HL-1) and in latemiddle-aged rat hearts. In HL-1 cells, we mimicked mitochondria-mediatedoxidative stress by treating cells with Antimycin A (AMA). AMA increasedmitochondrial superoxide generation, decreased mitochondrial membrane potential,increased nuclear DNA oxidation and decreased cellular respiration. Treatmentof HL-1 cells with the mTOR inhibitor rapamycin lead to a strong induction of autophagyand mitophagy and protected against the cytotoxic effects of AMA, assessed bycell survival and apoptotic signaling analysis. Rapamycin also preventedAMA-mediated increases in ubiquitinated protein aggregates. Autophagyinhibition attenuated the cytoprotective effects of rapamycin. For our in vivoexperiments, we investigated whether a late-life intervention of moderatecalorie restriction (CR, 20%) alone, or in combination with the plantpolyphenol resveratrol can induce autophagy in the hearts of late middle-agedrats. We further investigated whether such an induction of autophagy isprotective against the cardiotoxic effects of the chemotherapeutic drug doxorubicin,a known oxidative stressor. Our observed that CR and resveratrol, only whencombined, stimulated autophagic flux in the left ventricular tissue of latemiddle-aged rat hearts. Additionally, autophagy induction protected against thecytotoxic effects of doxorubicin, as assessed by apoptotic analysis in themyocardium and cardiac damage markers in serum. Our studies therefore suggestthat interventions aimed at enhancing basal autophagy may offer protectionagainst oxidative stress-mediated dysfunction in cardiomyocytes. ( en ) Advisors/Committee Members: Leeuwenburgh, Christiaan (committee chair), Aris, John P (committee member), Kim, Jae-Sung (committee member), Cousins, Robert J (committee member).

Subjects/Keywords: DNA damage; Gene therapy; Heart; Mitochondria; Mitochondrial DNA; Myocardium; Oxidative stress; Rats; Toxicity; Ubiquitins; autophagy  – cardiomyocytes  – oxidant

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

APA (6th Edition):

Dutta, D. (2012). The Role of Autophagy in Oxidative Stress-Mediated Dysfunction in Cardiac Cells and Rodent Hearts. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0044465

Chicago Manual of Style (16th Edition):

Dutta, Debapriya. “The Role of Autophagy in Oxidative Stress-Mediated Dysfunction in Cardiac Cells and Rodent Hearts.” 2012. Doctoral Dissertation, University of Florida. Accessed March 05, 2021. https://ufdc.ufl.edu/UFE0044465.

MLA Handbook (7th Edition):

Dutta, Debapriya. “The Role of Autophagy in Oxidative Stress-Mediated Dysfunction in Cardiac Cells and Rodent Hearts.” 2012. Web. 05 Mar 2021.

Vancouver:

Dutta D. The Role of Autophagy in Oxidative Stress-Mediated Dysfunction in Cardiac Cells and Rodent Hearts. [Internet] [Doctoral dissertation]. University of Florida; 2012. [cited 2021 Mar 05]. Available from: https://ufdc.ufl.edu/UFE0044465.

Council of Science Editors:

Dutta D. The Role of Autophagy in Oxidative Stress-Mediated Dysfunction in Cardiac Cells and Rodent Hearts. [Doctoral Dissertation]. University of Florida; 2012. Available from: https://ufdc.ufl.edu/UFE0044465


Universidade Estadual de Campinas

2. Inada, Natalia Mayumi. Ação fotodinamica de meso-porfirinas sobre função mitocondrial e viabilidade de celulas LNCaP: Photodynamic action of mesoporphyrins on mitochondrial functions and LNCaP cell viability.

Degree: 2006, Universidade Estadual de Campinas

Abstract: The action of irradiated cationic Fe(III)TMPyP and anionic Fe(III)TPPS4 forms of mesoporphyrins on mitochondrial functions was investigated using experimental conditions that caused minimal effects on mitochondria in the dark. Treatment of mitochondria with 1 µM Fe(III)TMPyP for 2 min decreased the respiratory control by 3% in the dark and 28% after irradiation. Fe(III)TPPS4 (1 µM) had no significant effect on respiratory control under any of the above conditions. Both porphyrins increased mitochondrial production of reactive oxygen species in the presence of Ca2+; however, the effect of Fe(III)TMPyP was significantly stronger. Fe(III)TMPyP but not Fe(III)TPPS4 promoted cyclosporin A-sensitive mitochondrial permeability transition. It was also observed that the association constant of Fe(III)TMPyP with mitochondria was 11 times higher than Fe(III)TPPS4. In conclusion, the damage to isolated mitochondria induced by Fe(III)TMPyP under illumination was larger than by Fe(III)TPPS4, probably because its cationic charge favors association with the mitochondrial membrane. The citotoxic effect of both porphyrins, prior the irradiation and upon the cell viability were dose-dependent and the IC50 were approximatly 15 µM, after 48 hours of incubation. No significantly cytotoxic effect was observed when the tumor cells were treated with 10 µM for each porphyrin, in a time of incubation in the dark of one hour. This was significant only after the photoactivation of the samples. In these conditions, the irradiation of the tumor cells induced cell death both via necrose and apoptose. Cell death via necrose was higher for both porphyrins. Irradiation of both porphyrins significantly increased the cytosolic Ca2+ concentration ([Ca2+]cit) of the LNCaP cells, which mediated cell death, once BAPTA/AM (an intracellular Ca2+ chelator) protected against cell death. Mitochondrial permeability transition (MPT) was probably participating in these mechanisms since cyclosporin A prevented cell death Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Vercesi, Anibal Eugenio, 1946- (advisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Fisiopatologia Médica (nameofprogram), Netto, Luis Eduardo Soares (committee member), Baptista, Mauricio da Silva (committee member), Saad, Sara Teresinha Olalla (committee member), Faria, Eliana Cotta de (committee member).

Subjects/Keywords: Mitocôndria; Oxigenio; Porfirinas; Bioenergética; Fotoquimioterapia; Agentes oxidantes; Mitochondria; Energy metabolism; Photodynamic therapy; Oxygen; Porphyrins; Oxidant agents

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

APA (6th Edition):

Inada, N. M. (2006). Ação fotodinamica de meso-porfirinas sobre função mitocondrial e viabilidade de celulas LNCaP: Photodynamic action of mesoporphyrins on mitochondrial functions and LNCaP cell viability. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/308197

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

Chicago Manual of Style (16th Edition):

Inada, Natalia Mayumi. “Ação fotodinamica de meso-porfirinas sobre função mitocondrial e viabilidade de celulas LNCaP: Photodynamic action of mesoporphyrins on mitochondrial functions and LNCaP cell viability.” 2006. Thesis, Universidade Estadual de Campinas. Accessed March 05, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308197.

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

MLA Handbook (7th Edition):

Inada, Natalia Mayumi. “Ação fotodinamica de meso-porfirinas sobre função mitocondrial e viabilidade de celulas LNCaP: Photodynamic action of mesoporphyrins on mitochondrial functions and LNCaP cell viability.” 2006. Web. 05 Mar 2021.

Vancouver:

Inada NM. Ação fotodinamica de meso-porfirinas sobre função mitocondrial e viabilidade de celulas LNCaP: Photodynamic action of mesoporphyrins on mitochondrial functions and LNCaP cell viability. [Internet] [Thesis]. Universidade Estadual de Campinas; 2006. [cited 2021 Mar 05]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/308197.

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

Council of Science Editors:

Inada NM. Ação fotodinamica de meso-porfirinas sobre função mitocondrial e viabilidade de celulas LNCaP: Photodynamic action of mesoporphyrins on mitochondrial functions and LNCaP cell viability. [Thesis]. Universidade Estadual de Campinas; 2006. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/308197

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


University of Toledo Health Science Campus

3. Zahedi, Shadi. Are Mitochondria a Potential Target for Anti-Cancer Therapy in Carcinoid Tumors?.

Degree: MSBS, College of Medicine, 2010, University of Toledo Health Science Campus

Gastrointestinal (GI) carcinoids are slow growing malignancies of neuroendocrine phenotype that can behave aggressively. To date, there are no effective therapies for metastatic carcinoid cancer. Previous work by our lab and others has shown that carcinoids express variety of voltage-operated (VOCCs) and non-voltage-operated Ca2+ channels to allow Ca2+ to enter the cell. Although, the role of Ca2+ entry in these tumors is not well understood, previous work by our group and others has shown that mitochondria are important regulators of voltage-operated and non-voltage-operated Ca2+ entry. In addition, cancer cells typically exhibit mitochondrial dysfunction and poor anti-oxidant status. These observations and the central role that mitochondria play in metabolism, Ca2+ homeostasis and cell death pathways make mitochondria an appealing potential target for anti-cancer treatment in carcinoid tumors. We used an spectrum of human cancer cell lines and a variety of microfluorescence methods including wide-field, confocal, and total internal reflection (TIRF) microscopy to assess Ca2+ signaling and mitochondrial function in combination with pharmacological interventions to assay whether mitochondria are a potential target for anti-cancer therapy. To this end, we tested the effectiveness of an oxidant therapy approach in carcinoid cells. Advisors/Committee Members: Giovannucci, David (Committee Chair).

Subjects/Keywords: Biomedical Research; Molecular Biology; Scientific Imaging; carcinoid tumors; mitochondrial; calcium signaling; TIRF microscopy; oxidant therapy; vitamin K3; vitamin C

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

APA (6th Edition):

Zahedi, S. (2010). Are Mitochondria a Potential Target for Anti-Cancer Therapy in Carcinoid Tumors?. (Masters Thesis). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1280427079

Chicago Manual of Style (16th Edition):

Zahedi, Shadi. “Are Mitochondria a Potential Target for Anti-Cancer Therapy in Carcinoid Tumors?.” 2010. Masters Thesis, University of Toledo Health Science Campus. Accessed March 05, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=mco1280427079.

MLA Handbook (7th Edition):

Zahedi, Shadi. “Are Mitochondria a Potential Target for Anti-Cancer Therapy in Carcinoid Tumors?.” 2010. Web. 05 Mar 2021.

Vancouver:

Zahedi S. Are Mitochondria a Potential Target for Anti-Cancer Therapy in Carcinoid Tumors?. [Internet] [Masters thesis]. University of Toledo Health Science Campus; 2010. [cited 2021 Mar 05]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1280427079.

Council of Science Editors:

Zahedi S. Are Mitochondria a Potential Target for Anti-Cancer Therapy in Carcinoid Tumors?. [Masters Thesis]. University of Toledo Health Science Campus; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1280427079

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