subject:(Neurotoxicity)

Northeastern University

1. Alsulimani, Helal. Effect of hemochromatosis on manganese neurotoxicity.

Degree: PhD, School of Pharmacy, 2017, Northeastern University

URL: http://hdl.handle.net/2047/D20261904

► Manganese (Mn) is an essential element for normal brain function, but excess levels of Mn in the brain are associated with a number of behavioral… (more)

Subjects/Keywords: hemochromatosis; manganese; neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Alsulimani, H. (2017). Effect of hemochromatosis on manganese neurotoxicity. (Doctoral Dissertation). Northeastern University. Retrieved from http://hdl.handle.net/2047/D20261904

Chicago Manual of Style (16^th Edition):

Alsulimani, Helal. “Effect of hemochromatosis on manganese neurotoxicity.” 2017. Doctoral Dissertation, Northeastern University. Accessed October 19, 2019. http://hdl.handle.net/2047/D20261904.

MLA Handbook (7^th Edition):

Alsulimani, Helal. “Effect of hemochromatosis on manganese neurotoxicity.” 2017. Web. 19 Oct 2019.

Vancouver:

Alsulimani H. Effect of hemochromatosis on manganese neurotoxicity. [Internet] [Doctoral dissertation]. Northeastern University; 2017. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/2047/D20261904.

Council of Science Editors:

Alsulimani H. Effect of hemochromatosis on manganese neurotoxicity. [Doctoral Dissertation]. Northeastern University; 2017. Available from: http://hdl.handle.net/2047/D20261904

Univerzitet u Beogradu

2. Martać, Ljiljana D., 1971-. Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom.

Degree: Biološki fakultet, 2014, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get

►

Neuronauke - neurofiziologija sa biofizikom / Neuroscience - neurophysiology and biophysics

Cilj ove teze je prikaz metoda za kvalitativnu i kvantitativnu analizu moždane aktivnosti. Ujedno… (more)

▼

Neuronauke - neurofiziologija sa biofizikom / Neuroscience - neurophysiology and biophysics

Cilj ove teze je prikaz metoda za kvalitativnu i kvantitativnu analizu moždane aktivnosti. Ujedno je matematički urađena biomedicinska aproksimacija rezultata. Animalni model intoksikacije aluminijumom je korišćen zbog rasprostranjenosti aluminijuma u prirodi i okruženju. Aluminijum ima selektivno neurotoksično dejstvo na pojedine delove mozga. Ujedno neurotoksičnost aluminijuma ima za posledicu izmenjenu aktivnost celog mozga, ali i specifično dejstvo na pojedine moždane funkcije. Animalni model nudi mogućnost više parametara i može se koristiti za izučavanje neurotoksičnosti aluminijuma pod različitim okolnostima. Procesi koji prate neurotoksičnost mogu se porediti sa promenama koje se javljaju u akutnim i hroničnim stanjima bolesti. Spektralna analiza zasnovana na Furijerovoj transformaciji daje opis promena elektrokortikalne aktivnosti po frekventnim oblastima. Poređenje spektara snage i njihova statistička analiza omogućavaju kvantifikaciju promena. Praćena je elektrokortikalna aktivnost parijetalnog korteksa i malog mozga kako bi se obuhvatila sva tri parametra intoksikacije: akumulacija u tkivu, lokalno izmenjena aktivnost neurona i promena regulatorne funkcije - plastičnost i adaptabilnost mozga. Eksperimentalni dizajn podrazumeva variranje parametara intoksikacije (aplikacija aluminijuma, moždana struktura, doza, starost, soj, fiziološko stanje). Na osnovu dobijenih podataka definisani su efekti neurotoksičnosti aluminijuma. Varijabilnost parametara fizioloških promena i efekata neurotoksičnosti su matematički analizirani. Rezultati ukazuju da promena moždane aktivnosti može biti graduisana tako da može poslužiti kao dijagnostičko-prognostički parametar patofiziološkog stanja. Ova studija ima multidisciplinarni značaj jer obrađuje različite aspekte - biološki, fiziološki i medicinski.

Advisors/Committee Members: Radenović, Lidija, 1966-.

Subjects/Keywords: neurotoxicity; electrophysiology; spectral analysis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Martać, Ljiljana D., 1. (2014). Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get

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):

Martać, Ljiljana D., 1971-. “Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom.” 2014. Thesis, Univerzitet u Beogradu. Accessed October 19, 2019. https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Martać, Ljiljana D., 1971-. “Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom.” 2014. Web. 19 Oct 2019.

Vancouver:

Martać, Ljiljana D. 1. Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom. [Internet] [Thesis]. Univerzitet u Beogradu; 2014. [cited 2019 Oct 19]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get.

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

Council of Science Editors:

Martać, Ljiljana D. 1. Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom. [Thesis]. Univerzitet u Beogradu; 2014. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get

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

University of New South Wales

3. Park, Susanna Beatrice. The pathophysiology of chemotherapy-induced neurotoxicity.

Degree: Clinical School - Prince of Wales Hospital, 2010, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/50327 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9208/SOURCE02?view=true

► This thesis examines the pathophysiology underlying chemotherapy-induced neurotoxicity. Oxaliplatin, utilised in the treatment of colorectal cancer, produces prominent neurotoxicity. Clinical and specialised neurophysiological studies were… (more)

▼ This thesis examines the pathophysiology underlying chemotherapy-induced neurotoxicity. Oxaliplatin, utilised in the treatment of colorectal cancer, produces prominent neurotoxicity. Clinical and specialised neurophysiological studies were undertaken to determine the full spectrum of oxaliplatin-induced neuropathy. These studies demonstrated acute alterations in Na+ channel-related parameters in sensory axons post-infusion, suggesting that an acute Na+ channelopathy may contribute to the development of neuropathic symptoms. Patients were also assessed longitudinally, revealing a characteristic pattern of sensory axonal abnormalities, which developed progressively across treatment and occurred earlier than changes in conventional parameters of nerve function. Importantly, excitability abnormalities were predictive of neuropathy severity at treatment completion. Studies in a subset of oxaliplatin-treated patients with Lhermitte's phenomenon (electric shock-like sensations on neck flexion) confirmed that the extent of excitability change was associated with the severity of neuropathy. To further define mechanisms, studies were undertaken before and immediately following oxaliplatin infusion. These studies established that oxaliplatin affected transient Na+ channel inactivation processes more significantly than persistent Na+ channel conductances in both motor and sensory axons. Studies utilising natural activity to produce axonal hyperpolarization established that changes in the recovery cycle of excitability post-oxaliplatin were greatly enhanced. These studies established that oxaliplatin-induced changes were membrane-potential dependent, supporting the hypothesis that oxaliplatin modulates axonal Na+ channel inactivation. To examine the long-term sequelae of oxaliplatin treatment, follow-up studies were undertaken, revealing chronic sensory neuropathy in the majority of patients. Importantly, sensory axonal excitability measures prospectively obtained during treatment were predictive of neurological outcomes at long-term follow-up, confirming that excitability techniques provided a sensitive biomarker of oxaliplatin-induced neuropathy. To contrast these findings, a cohort of paclitaxel-treated patients were assessed, revealing an entirely different basis for neurotoxicity related to damaged axonal transport systems. Paclitaxel produced early and progressive changes in stimulus threshold and maximal sensory amplitudes in the absence of focal changes in individual axonal conductances. In conclusion, studies in this thesis have established abnormalities in selective axonal Na+ channel-dependent properties in oxaliplatin-treated patients which preceded the development of neuropathy. Axonal excitability techniques may be utilised as early and sensitive biomarkers of oxaliplatin-induced neurotoxicity, yielding important insight into pathophysiological mechanisms of neuropathy. Advisors/Committee Members: Kiernan, Matthew C., Clinical School - Prince of Wales Hospital, Faculty of Medicine, UNSW, Lin, Cindy S-Y., Medical Sciences, Faculty of Medicine, UNSW.

Subjects/Keywords: Neuropathy; Neurology; Neurotoxicity; Chemotherapy; Oxaliplatin

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Park, S. B. (2010). The pathophysiology of chemotherapy-induced neurotoxicity. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/50327 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9208/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Park, Susanna Beatrice. “The pathophysiology of chemotherapy-induced neurotoxicity.” 2010. Doctoral Dissertation, University of New South Wales. Accessed October 19, 2019. http://handle.unsw.edu.au/1959.4/50327 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9208/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Park, Susanna Beatrice. “The pathophysiology of chemotherapy-induced neurotoxicity.” 2010. Web. 19 Oct 2019.

Vancouver:

Park SB. The pathophysiology of chemotherapy-induced neurotoxicity. [Internet] [Doctoral dissertation]. University of New South Wales; 2010. [cited 2019 Oct 19]. Available from: http://handle.unsw.edu.au/1959.4/50327 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9208/SOURCE02?view=true.

Council of Science Editors:

Park SB. The pathophysiology of chemotherapy-induced neurotoxicity. [Doctoral Dissertation]. University of New South Wales; 2010. Available from: http://handle.unsw.edu.au/1959.4/50327 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9208/SOURCE02?view=true

4. Frimat, Jean-Philippe. Cell patterning for spatially standardized cell biology.

Degree: 2011, Technische Universität Dortmund

URL: http://hdl.handle.net/2003/29385

► The onus in modern cell biology is on the development of reproducible, develop cell patterning capabilities that are accessible to biologists and to demonstrate new… (more)

Subjects/Keywords: Cell patterning; Microfluidics; Neurotoxicity; Spheroids; 660

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Frimat, J. (2011). Cell patterning for spatially standardized cell biology. (Thesis). Technische Universität Dortmund. Retrieved from http://hdl.handle.net/2003/29385

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):

Frimat, Jean-Philippe. “Cell patterning for spatially standardized cell biology.” 2011. Thesis, Technische Universität Dortmund. Accessed October 19, 2019. http://hdl.handle.net/2003/29385.

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

MLA Handbook (7^th Edition):

Frimat, Jean-Philippe. “Cell patterning for spatially standardized cell biology.” 2011. Web. 19 Oct 2019.

Vancouver:

Frimat J. Cell patterning for spatially standardized cell biology. [Internet] [Thesis]. Technische Universität Dortmund; 2011. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/2003/29385.

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

Council of Science Editors:

Frimat J. Cell patterning for spatially standardized cell biology. [Thesis]. Technische Universität Dortmund; 2011. Available from: http://hdl.handle.net/2003/29385

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

Humboldt State University

5. Hedges, Kathryn A. Copper exposure damages neurons and induces paralysis in the nematode, Caenorhabditis elegans, far below lethal concentrations.

Degree: MA, Biology, 2010, Humboldt State University

URL: http://hdl.handle.net/2148/608

► This study examined the effects of copper exposure on neurons and the excretory cell in the nematode, Caenorhabditis elegans, using transgenic strains with specific green… (more)

Subjects/Keywords: Copper; Neurotoxicity; Invertebrates; Dopamine; GABA; Excretory cell

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hedges, K. A. (2010). Copper exposure damages neurons and induces paralysis in the nematode, Caenorhabditis elegans, far below lethal concentrations. (Masters Thesis). Humboldt State University. Retrieved from http://hdl.handle.net/2148/608

Chicago Manual of Style (16^th Edition):

Hedges, Kathryn A. “Copper exposure damages neurons and induces paralysis in the nematode, Caenorhabditis elegans, far below lethal concentrations.” 2010. Masters Thesis, Humboldt State University. Accessed October 19, 2019. http://hdl.handle.net/2148/608.

MLA Handbook (7^th Edition):

Hedges, Kathryn A. “Copper exposure damages neurons and induces paralysis in the nematode, Caenorhabditis elegans, far below lethal concentrations.” 2010. Web. 19 Oct 2019.

Vancouver:

Hedges KA. Copper exposure damages neurons and induces paralysis in the nematode, Caenorhabditis elegans, far below lethal concentrations. [Internet] [Masters thesis]. Humboldt State University; 2010. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/2148/608.

Council of Science Editors:

Hedges KA. Copper exposure damages neurons and induces paralysis in the nematode, Caenorhabditis elegans, far below lethal concentrations. [Masters Thesis]. Humboldt State University; 2010. Available from: http://hdl.handle.net/2148/608

University of Debrecen

6. Sakian, Yehonatan. 'Pharmacological Treatment of ALS' .

Degree: DE – Általános Orvostudományi Kar, 2014, University of Debrecen

URL: http://hdl.handle.net/2437/194938

► The Article deals with the Progressive Neurodegenerative Disease ALS. It includes general background on the pathogenesis, clinical features, genetics and epidemiology. The main goal is… (more)

Subjects/Keywords: ALS; Rilozule; Pharmacotherapy; Gacyclidine; Dexpramipexole; Neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Sakian, Y. (2014). 'Pharmacological Treatment of ALS' . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/194938

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):

Sakian, Yehonatan. “'Pharmacological Treatment of ALS' .” 2014. Thesis, University of Debrecen. Accessed October 19, 2019. http://hdl.handle.net/2437/194938.

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

MLA Handbook (7^th Edition):

Sakian, Yehonatan. “'Pharmacological Treatment of ALS' .” 2014. Web. 19 Oct 2019.

Vancouver:

Sakian Y. 'Pharmacological Treatment of ALS' . [Internet] [Thesis]. University of Debrecen; 2014. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/2437/194938.

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

Council of Science Editors:

Sakian Y. 'Pharmacological Treatment of ALS' . [Thesis]. University of Debrecen; 2014. Available from: http://hdl.handle.net/2437/194938

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

Virginia Tech

7. Jiang, Ying. Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species.

Degree: MS, Entomology, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/41236

► Malaria (vector: Anopheles gambiae) is a major infectious disease that kills about 1 million people each year. For the improvement of its treatment and vector… (more)

▼ Malaria (vector: Anopheles gambiae) is a major infectious disease that kills about 1 million people each year. For the improvement of its treatment and vector control during the past decades, several issues such as high medicine cost, insecticide resistance, and lack of an effective vaccine have prevented adequate control of malaria. Additionally, the low selectivity of malaria vector insecticides also presents a public health problem. The purpose of developing novel carbamate insecticides in our laboratory is to offer effective and selective insecticide options to achieve the ultimate goal of malaria control. First, 50% inhibition concentration (IC50) data was collected from three mammalian AChEs with eight commercial carbamate insecticides by using the Ellman assay. The IC50 values varied from 57 nM to 7358 nM. The AChE sensitivity pattern and level were shown to be similar between the recombinant mouse and ICR male mouse brain cortex homogenate (slope = 0.99, R2 = 0.96). Then eight novel carbamate insecticides that are possible malaria vector control agents were selected for further neurotoxicity testing in non-target organisms. For commercial carbamate insecticides, the IC50 varied from 9.1 nM to 2,094 nM. For the novel carbamate insecticides, it varied from 58 nM to 388,800 nM. Based on IC50 data from previous work on A. gambiae, the selectivity index (IC50 of non-target species / IC50 A. gambiae) ranged from 0.17 to 5.64 and from 0.47 to 19,587 for commercial and novel carbamate insecticides, respectively. Subsequently, the AChE protein sequence alignment comparison and cladogram were used to compare the genetic and evolutionary relationship among five different organisms. The alignment score ranged from 88 for mouse vs. human to 54 for hen vs. T. californica. The evolutionary relationships among species was obtained from the cladogram. Recombinant mouse vs. recombinant human was shown to have the most similar inhibitor potency profiles (alignment score = 88, closest taxa position on cladogram, similar AChE sensitivity pattern [R2 = 0.81] and level [P > 0.05] to the novel carbamates). Neurotoxic esterase (NTE) assay showed that the novel carbamates did not significantly inhibit NTE, inhibition of which underlies a significant hazard for anticholinesterases, especially organophosphates, in several nontarget vertebrate organisms. The NTE activity in the presence of novel carbamate insecticides ranged from 93% to 116% of the control, while in the commercial group, bendiocarb significantly inhibited NTE, leaving only 76.5% of the initial reactivity at 1 mM inhibitor concentration. Further in vivo bioassay using Daphnia magna was conducted to compare the aquatic toxicity of commercial and novel carbamates. The data showed that except for PRC331 (3-tert-butylphenylmethylcarbamate), all novel carbamates were of similar potency as bendiocarb (LC50 = 611 nM) for aquatic toxicity, and their LC50 values ranged from 172 nM (PRC331) to 1109 nM. In conclusion, the novel carbamate insecticides would… Advisors/Committee Members: Bloomquist, Jeffrey R. (committeechair), Carlier, Paul R. (committee member), Mullins, Donald E. (committeecochair).

Subjects/Keywords: neurotoxic esterase; acetylcholinesterase; carbamate insecticides; neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Jiang, Y. (2011). Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/41236

Chicago Manual of Style (16^th Edition):

Jiang, Ying. “Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species.” 2011. Masters Thesis, Virginia Tech. Accessed October 19, 2019. http://hdl.handle.net/10919/41236.

MLA Handbook (7^th Edition):

Jiang, Ying. “Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species.” 2011. Web. 19 Oct 2019.

Vancouver:

Jiang Y. Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species. [Internet] [Masters thesis]. Virginia Tech; 2011. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10919/41236.

Council of Science Editors:

Jiang Y. Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species. [Masters Thesis]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/41236

Virginia Tech

8. Freeborn, Ethan Ray. The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease.

Degree: MS, Entomology, 1999, Virginia Tech

URL: http://hdl.handle.net/10919/9769

► Epidemiological and analytical studies have suggested that environmental exposure to neurotoxic insecticides may exist as a factor in the etiology of Parkinson's Disease (PD). This… (more)

Subjects/Keywords: stiatum; insecticides; neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Freeborn, E. R. (1999). The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/9769

Chicago Manual of Style (16^th Edition):

Freeborn, Ethan Ray. “The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease.” 1999. Masters Thesis, Virginia Tech. Accessed October 19, 2019. http://hdl.handle.net/10919/9769.

MLA Handbook (7^th Edition):

Freeborn, Ethan Ray. “The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease.” 1999. Web. 19 Oct 2019.

Vancouver:

Freeborn ER. The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease. [Internet] [Masters thesis]. Virginia Tech; 1999. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10919/9769.

Council of Science Editors:

Freeborn ER. The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease. [Masters Thesis]. Virginia Tech; 1999. Available from: http://hdl.handle.net/10919/9769

University of Ottawa

9. Campbell, Sonja Gray. Methylmercury Neurotoxicity and Interactions with Selenium .

Degree: 2015, University of Ottawa

URL: http://hdl.handle.net/10393/33173

► Methylmercury (MeHg) is a ubiquitous contaminant and potent neurotoxicant with no completely effective therapy, although selenium antagonises MeHg toxicity. Furthermore, nanoparticles are promising as a… (more)

Subjects/Keywords: Astrocyte; Mercury; Methylmercury; Nanoparticle; Neurotoxicity; Selenium

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Campbell, S. G. (2015). Methylmercury Neurotoxicity and Interactions with Selenium . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/33173

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):

Campbell, Sonja Gray. “Methylmercury Neurotoxicity and Interactions with Selenium .” 2015. Thesis, University of Ottawa. Accessed October 19, 2019. http://hdl.handle.net/10393/33173.

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

MLA Handbook (7^th Edition):

Campbell, Sonja Gray. “Methylmercury Neurotoxicity and Interactions with Selenium .” 2015. Web. 19 Oct 2019.

Vancouver:

Campbell SG. Methylmercury Neurotoxicity and Interactions with Selenium . [Internet] [Thesis]. University of Ottawa; 2015. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10393/33173.

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

Council of Science Editors:

Campbell SG. Methylmercury Neurotoxicity and Interactions with Selenium . [Thesis]. University of Ottawa; 2015. Available from: http://hdl.handle.net/10393/33173

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

University of Minnesota

10. Brunner, Angela Haijung. Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery.

Degree: PhD, Pharmacology, 2013, University of Minnesota

URL: http://purl.umn.edu/152561

► HIV infection is a worldwide pandemic. A debilitating neurological consequence of HIV infection is progressive cognitive decline, known as HIV-associated neurocognitive disorders (HAND). HAND afflicts… (more)

▼ HIV infection is a worldwide pandemic. A debilitating neurological consequence of HIV infection is progressive cognitive decline, known as HIV-associated neurocognitive disorders (HAND). HAND afflicts up to 50% of all HIV patients to varying degrees, and as survival of HIV patients improves with current antiretroviral therapies, the prevalence of HAND is also increasing. This, coupled with the lack of current effective HAND therapies, creates a dire need to understand the mechanisms underlying the cognitive decline associated with HIV. HAND symptoms correlate closely with processes of neuronal injury, which are early events that precede overt neuronal death. One such injurious process is synapse loss. The HIV protein transactivator of transcription (Tat) is a neurotoxic viral protein released from infected cells into the central nervous system. Tat contributes to the pathologies seen in HAND patients, and induces loss of excitatory synapses between rat hippocampal neurons in culture. Using an innovative live cell imaging assay, our laboratory has previously shown that Tat induces reversible synapse loss via a pathway that is distinct from cell death. In this dissertation, I outline three studies that stem from the current knowledge involving Tat-induced synapse loss. These studies elucidated important information regarding the mechanisms by which HIV Tat exerts its neurotoxic effects, emphasizing the importance of subunit composition when determining toxic or beneficial effects of NMDA receptor activation as well as unmasking the importance of the postsynaptic density as the central target of Tat's effects. Furthermore, these studies highlight the reversibility of synapse loss and uncover a new role for the canonical NO/cGMP/PKG pathway in modulating synapse recovery downstream of GluN2B-containing NMDA receptors. Tat-induced synapse loss and subsequent recovery can correlate to symptoms of cognitive decline seen in HAND. Targeting these mechanisms can shed new light on therapeutic strategies to treat HAND patients.

Subjects/Keywords: HIV; Neurotoxicity; NMDA; Pharmacology; Synapse; Tat

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Brunner, A. H. (2013). Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/152561

Chicago Manual of Style (16^th Edition):

Brunner, Angela Haijung. “Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery.” 2013. Doctoral Dissertation, University of Minnesota. Accessed October 19, 2019. http://purl.umn.edu/152561.

MLA Handbook (7^th Edition):

Brunner, Angela Haijung. “Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery.” 2013. Web. 19 Oct 2019.

Vancouver:

Brunner AH. Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery. [Internet] [Doctoral dissertation]. University of Minnesota; 2013. [cited 2019 Oct 19]. Available from: http://purl.umn.edu/152561.

Council of Science Editors:

Brunner AH. Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery. [Doctoral Dissertation]. University of Minnesota; 2013. Available from: http://purl.umn.edu/152561

University of Arizona

11. Herndon, Joseph Menzel. Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia .

Degree: 2013, University of Arizona

URL: http://hdl.handle.net/10150/306920

► 3,4-(±)-Methylenedioxymethamphetamine (MDMA, ecstasy) is a widely abused amphetamine derivative. The metabolism of MDMA is thought to be a necessary component of MDMA-induced neurotoxicity, as direct… (more)

▼ 3,4-(±)-Methylenedioxymethamphetamine (MDMA, ecstasy) is a widely abused amphetamine derivative. The metabolism of MDMA is thought to be a necessary component of MDMA-induced neurotoxicity, as direct administration of MDMA into the central nervous system of rats failed to reproduce the hallmark serotonin deficits seen following systemic administration of MDMA. Mechanistic questions remain regarding how MDMA elicits this neurotoxicity. Work of this thesis was undertaken to examine how MDMA-induced neurotoxicity is affected by the activity of two polymorphic enzymes involved in the metabolism of MDMA, namely cytochrome P450 family member 2D6 (CYP2D6) and catechol-O-methyltransferase (COMT), as well as the potential role microglia play in the facilitation of this neurotoxicity. Inhibition of CYP2D1, the homolog of human CYP2D6 in the rat, resulted in an attenuation of serotonergic neurotoxicity following MDMA-administration. In both a pharmacological model and a genetic model of CYP2D1 inhibition, serotonin deficits were alleviated when compared to normal-activity CYP2D1 counterparts. Inhibition of COMT, the primary detoxication enzyme in the MDMA pathway, resulted in potentiation of MDMA-induced neurotoxicity. In a pharmacological model of COMT inhibition, rats displayed greater long-term serotonin deficits after COMT inhibition. Mice devoid of COMT proved sensitive to the lethal hyperthermic effects of MDMA, illustrating the importance of this enzyme in preventing the acute toxicity of MDMA. Brain lesions often elicit a microglial response. Microglia have the potential of both beneficial and deleterious actions in the brain. Whether microglia are activated by nerve terminal degeneration produced by MDMA is an area of ongoing debate. Systemically delivered MDMA produces a modest increase in the amount of microglial cells present in the parietal cortex of rats over a one-week period. MDMA also increased the phagocytic activity of microglia in the cortex. The studies described herein support the hypothesis that metabolism is critical in MDMA-induced neurotoxicity. Furthermore, as both CYP2D6 and COMT are polymorphic in the human population, certain individuals are more at risk for severe serotonergic toxicity following MDMA administration. Finally, while microglia are likely not the cause of MDMA-induced neurotoxicity, contributions of these cells cannot be dismissed. Advisors/Committee Members: Monks, Terrence J (advisor), Monks, Terrence J. (committeemember), Lau, Serrine S. (committeemember), Lai, Josephine Y. (committeemember), Wright, Stephen H. (committeemember), Cherrington, Nathan J. (committeemember).

Subjects/Keywords: CYP2D6; MDMA; Microglia; Neurotoxicity; Pharmacology & Toxicology; COMT

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Herndon, J. M. (2013). Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/306920

Chicago Manual of Style (16^th Edition):

Herndon, Joseph Menzel. “Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia .” 2013. Doctoral Dissertation, University of Arizona. Accessed October 19, 2019. http://hdl.handle.net/10150/306920.

MLA Handbook (7^th Edition):

Herndon, Joseph Menzel. “Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia .” 2013. Web. 19 Oct 2019.

Vancouver:

Herndon JM. Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia . [Internet] [Doctoral dissertation]. University of Arizona; 2013. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10150/306920.

Council of Science Editors:

Herndon JM. Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia . [Doctoral Dissertation]. University of Arizona; 2013. Available from: http://hdl.handle.net/10150/306920

12. Zahir, Farhana. Neurotoxicity of organic mercury in albino rats; -.

Degree: Zoology, 2003, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/51690

Abstract available newline newline

Bibliography p. 139-177

Advisors/Committee Members: Rizvi, Shamim J and Jairajpuri, Durdana S.

Subjects/Keywords: Neurotoxicity; Organic; Mercury; Albino

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Zahir, F. (2003). Neurotoxicity of organic mercury in albino rats; -. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/51690

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):

Zahir, Farhana. “Neurotoxicity of organic mercury in albino rats; -.” 2003. Thesis, Aligarh Muslim University. Accessed October 19, 2019. http://shodhganga.inflibnet.ac.in/handle/10603/51690.

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

MLA Handbook (7^th Edition):

Zahir, Farhana. “Neurotoxicity of organic mercury in albino rats; -.” 2003. Web. 19 Oct 2019.

Vancouver:

Zahir F. Neurotoxicity of organic mercury in albino rats; -. [Internet] [Thesis]. Aligarh Muslim University; 2003. [cited 2019 Oct 19]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51690.

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

Council of Science Editors:

Zahir F. Neurotoxicity of organic mercury in albino rats; -. [Thesis]. Aligarh Muslim University; 2003. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51690

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

University of Utah

13. Elayan, Ikram Mohammad. Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;.

Degree: PhD, Pharmacology & Toxicology;, 1994, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592

► Systemic administration of methamphetamine (Meth) causes neurochemical deficits in terminals of the nigrostriatal dopaminergic system. The mechanism by which Meth causes this neurotoxicity is still… (more)

▼ Systemic administration of methamphetamine (Meth) causes neurochemical deficits in terminals of the nigrostriatal dopaminergic system. The mechanism by which Meth causes this neurotoxicity is still not known. Several investigators have suggested that the excitatory neurotransmitter, glutamate (Glu), participates in mediating this neurotoxicity. The current study was conducted to investigate the role of Meth on Glu release by utilizing both in vitro and in vivo systems. Incubation of glutamatergic neurons with Meth in vitro failed to release Glu from these neurons. Also, perfusing striatal slices with Meth, in vitro, failed to release Glu from these slices. These results suggested that a complete neuronal circuit might be needed in order for Meth to affect Glu release in the striatum. Therefore, in vivo microdialysis techniques were utilized to investigate the release of Glu in the striatum. No difference was observed in Glu levels in perfusates of animals treated with a single dose of Meth, administered ten minutes after a single dose of iprindole, in comparison to control animals. When DL-threo-/beta-hydroxyaspartic acid, a Glu uptake blocker, was given with Meth, Glu concentrations in striatal dialysate of rats treated with Meth + blocker were significantly higher than those in the blocker alone-treated group. These higher levels of striatal Glu in response to Meth treatment may contribute to Meth neurotoxicity since Glu causes neurotoxicity. Perfusion of the Glu uptake blocker alone into the striatum increased Glu levels in the extracellular space. These levels of Glu were maintained only for 1 h and then declined to almost 50% of the peak value even though the blocker was continuously administered through the dialysis probe. Haloperidol, a dopamine D2 receptor antagonist, and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)-quinoxaline (NBQX), a non-N-methyl-D-aspartic acid (NMDA) Glu receptor antagonist, partially inhibited this decline in Glu levels. These results may be due to an inhibitory effect of dopamine on Glu release in the striatum through a D2 receptor. The finding that NBQX partially blocked this decline in Glu levels raises the possibility of an inhibitory non-NMDA autoreceptor on the corticostriatal pathway. The Glu uptake blocker alone also increased extracellular DA levels in the striatum, which is the first report of this phenomenon.

Subjects/Keywords: Neurotoxicity; Cerebellar Granule Cells

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Elayan, I. M. (1994). Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592

Chicago Manual of Style (16^th Edition):

Elayan, Ikram Mohammad. “Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;.” 1994. Doctoral Dissertation, University of Utah. Accessed October 19, 2019. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592.

MLA Handbook (7^th Edition):

Elayan, Ikram Mohammad. “Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;.” 1994. Web. 19 Oct 2019.

Vancouver:

Elayan IM. Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;. [Internet] [Doctoral dissertation]. University of Utah; 1994. [cited 2019 Oct 19]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592.

Council of Science Editors:

Elayan IM. Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;. [Doctoral Dissertation]. University of Utah; 1994. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592

Universidade do Rio Grande do Sul

14. Mello, Fabíola Peixoto da Silva. Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar.

Degree: 2011, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/29045

►

Os meios de contraste iodados são substâncias radiopacas utilizadas em mielografias e, muito embora o iohexol e o iopamidol sejam considerados seguros na rotina mielográfica… (more)

▼

Os meios de contraste iodados são substâncias radiopacas utilizadas em mielografias e, muito embora o iohexol e o iopamidol sejam considerados seguros na rotina mielográfica de humanos e animais, eventos adversos são relacionados ao seu uso. O iobitridol foi desenvolvido mais recentemente, sendo seu desenho molecular obtido após pesquisas sobre a conformação, distribuição e natureza permanente da estrutura hidrofílica; no entanto, estudos referentes à neurotoxicidade do iobitridol com administração subaracnóide são escassos e inconclusivos. O objetivo do presente trabalho foi comparar a neurotoxicidade do iobitridol com a do iohexol, por via intracisternal em ratos Wistar, como avaliação pré-clínica da utilização deste como agente mielográfico. Foram utilizados 75 animais divididos em três grupos experimentais de 25 animais: iobitridol, iohexol e NaCl 0,9% (grupo controle), e; estes subdivididos em cinco subgrupos com cinco animais cada, com doses distintas de 200, 400, 600, 800 e 1000 mg I/kg, sendo utilizado no grupo controle o volume equivalente aos meios de contraste testados. Os animais foram avaliados no momento da aplicação do iohexol e iobitridol quanto a alterações do trato respiratório, e posteriormente, aos 5, 15, 30, 60, 120, 180 e 240 minutos após este procedimento, quanto a sinais de depressão e excitação, reflexos tátil de agarramento palmar, flexor, extensor, palpebral, pupilar e da pina, reação de endireitamento e posicionamento e resposta auditiva. Nos sete dias subseqüentes, foram avaliados diariamente quanto a estes parâmetros, e ainda mensurados o peso e a ingestão de ração e de água. Não foram observadas diferenças estatisticamente significativas entre os grupos testados com meios de contraste, em nenhum dos parâmetros avaliados. Nesse modelo animal o iobitridol demonstrou baixa neurotoxicidade, comparável a observada com o iohexol, tornando-o uma possibilidade alternativa para utilização pela via subaracnóidea para realização de mielografias.

The iodinated contrast agents are radiopaque substances used in myelography, and although the iohexol and iopamidol are considered safe in human and animal myelographic routine, adverse events are related to their use. The iobitridol was recently developed, and its molecular designs obtained after research on the configuration, distribution and permanent nature of hydrophilic structure; however, neurotoxicologic studies of iobitridol in subarachnoid administration are scarce and inconclusive. The purpose of this study was to compare the neurotoxicity of iobitridol with iohexol, by intracisternal administration in Wistar rats, as pre-clinical evaluation of the use of this substance as myelographic agent. Seventy five animals were used, divided into three experimental groups with twenty five animals: iobitridol, iohexol and NaCl 0,9% (control group); and they are divided into five subgroups of five animals each, with different doses of 200, 400, 600, 800 and 1000 mg I/kg, while the control group received the equivalent volume of contrast media tested.…

Advisors/Committee Members: Mello, Joao Roberto Braga de.

Subjects/Keywords: Contrast media; Farmacologia veterinaria; Iobitridol; Neurotoxicidade; Mielografia; Iohexol; Neurotoxicity; Intracisternal; Myelography

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Mello, F. P. d. S. (2011). Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/29045

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):

Mello, Fabíola Peixoto da Silva. “Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar.” 2011. Thesis, Universidade do Rio Grande do Sul. Accessed October 19, 2019. http://hdl.handle.net/10183/29045.

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

MLA Handbook (7^th Edition):

Mello, Fabíola Peixoto da Silva. “Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar.” 2011. Web. 19 Oct 2019.

Vancouver:

Mello FPdS. Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2011. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10183/29045.

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

Council of Science Editors:

Mello FPdS. Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar. [Thesis]. Universidade do Rio Grande do Sul; 2011. Available from: http://hdl.handle.net/10183/29045

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

15. Spampinato, Simona Federica. Interaction between estrogen receptor and metabotropic glutamate receptor 1 mediates the dual effect of estrogen in neuroprotection and neurodegeneration.

Degree: 2012, Università degli Studi di Catania

URL: http://hdl.handle.net/10761/983

► Estrogen receptors (ER) are known to exert important action in the central nervous system, including neuroprotection. These effects are due to interaction of estrogen with… (more)

▼ Estrogen receptors (ER) are known to exert important action in the central nervous system, including neuroprotection. These effects are due to interaction of estrogen with membrane localized receptors that signal through rapid transduction pathways. How membrane ERs initiate rapid signal transduction has not been clarified, but they have been reported to interact with other membrane receptors, including metabotropic glutamate receptors (mGluR). The role of estrogen in neuroprotection is not always defined and above all, neuroprotective data provided by preclinical studies have not been confirmed by the use of estrogen in humans: estrogen treatment can in fact be neuroprotective but also responsible for increased neurodegeneration. The dual role ascribed to estrogen, can be observed also with mGluR1 agonists. 3,5-Dihydroxyphenylglycine (DHPG) behaves both as a neuroprotective and neurodegenerative factor. The aim of this study has been to point out whether the similar behaviour of the estrogen and mGlu1R agonists depends on the interaction between their receptors. Neuroprotective activity of both drugs was demonstrated in an in vitro model of cortical cultures exposed to beta amyloid (Aâ) toxicity. Pre-treatment with either 17â-estradiol (E2) and DHPG reduced Aâ-induced neuronal death. The neuroprotective effect was due to strict interaction between mGluR1 and ERá, as treatment with the mGluR1 antagonist, JNJ 16259685, or ER antagonist, ICI 182,780, prevented the effect induced by the respective as well as by the reciprocal agonist. Moreover, E2 and DHPG shared a common signalling pathway, as they stimulated to a similar extent phosphoinositide hydrolysis and induced enhanced phosphorylation of AKT. Both these effects were not additive, when the two agonists were added together and they were prevented by the reciprocal antagonists. In addition, a similar effect was reproduced when each receptor was expressed in recombinant cells. The interaction between the two receptors seems to be involved also in the neurotoxic effect of E2 and DHPG. Both compounds exacerbated NMDA induced toxicity when added after the neurotoxic challenge, while being still neuroprotective when administered before. The effect of E2 was not modified by co-treatment with DHPG and was sensitive to ICI 182,780, but also to JNJ16259685. Moreover, this potentiating effect is abolished by pre-treatment with a calpain III inhibitor. The ability of E2 to phosphorylate AKT and ERK is reduced after NMDA pulse, but this effect is partially reverted by pre-treatment with the calpain inhibitor. Altogether the present data demonstrate that membrane ERs and mGluR1 interact to induce both neuroprotection and neurodegeneration. The different outcome may depend on the cellular conditions, thus pointing out the importance of the choice of the timing of intervention.

Subjects/Keywords: Area 05 - Scienze biologiche; Estrogen, neuroprotection, metabotropic glutamate receptors, neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Spampinato, S. F. (2012). Interaction between estrogen receptor and metabotropic glutamate receptor 1 mediates the dual effect of estrogen in neuroprotection and neurodegeneration. (Thesis). Università degli Studi di Catania. Retrieved from http://hdl.handle.net/10761/983

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):

Spampinato, Simona Federica. “Interaction between estrogen receptor and metabotropic glutamate receptor 1 mediates the dual effect of estrogen in neuroprotection and neurodegeneration.” 2012. Thesis, Università degli Studi di Catania. Accessed October 19, 2019. http://hdl.handle.net/10761/983.

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

MLA Handbook (7^th Edition):

Spampinato, Simona Federica. “Interaction between estrogen receptor and metabotropic glutamate receptor 1 mediates the dual effect of estrogen in neuroprotection and neurodegeneration.” 2012. Web. 19 Oct 2019.

Vancouver:

Spampinato SF. Interaction between estrogen receptor and metabotropic glutamate receptor 1 mediates the dual effect of estrogen in neuroprotection and neurodegeneration. [Internet] [Thesis]. Università degli Studi di Catania; 2012. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10761/983.

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

Council of Science Editors:

Spampinato SF. Interaction between estrogen receptor and metabotropic glutamate receptor 1 mediates the dual effect of estrogen in neuroprotection and neurodegeneration. [Thesis]. Università degli Studi di Catania; 2012. Available from: http://hdl.handle.net/10761/983

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

University of Plymouth

16. Xiaoqing, Liu. Dose-banding studies on oxaliplatin.

Degree: PhD, 2016, University of Plymouth

URL: http://hdl.handle.net/10026.1/8081

► Oxaliplatin is an anticancer drug widely used in cancer chemotherapy. This thesis evaluates whether a specific dose-banding scheme for oxaliplatin could replace the individual dosing… (more)

▼ Oxaliplatin is an anticancer drug widely used in cancer chemotherapy. This thesis evaluates whether a specific dose-banding scheme for oxaliplatin could replace the individual dosing method that is currently used in the oxaliplatin administration. Dose-banding was introduced into UK clinical practice in 2001, as it reduces delays in patients receiving their treatment and, through quality control and end-product testing, safeguards the infusion quality and patient safety. A range of studies were included in this thesis: an extended stability study on oxaliplatin infusions using a sequential temperature cycling design; studies on oxalate, a potential degradation product and metabolite of oxaliplatin which has been linked to oxaliplatin neurotoxicity and the development of an ex vivo pharmacokinetic (PK) simulation model to compare the effect of different oxaliplatin dosing methods on its therapeutic outcomes. The shelf-life of oxaliplatin infusions over a concentration range of 0.2 mg/mL – 0.7 mg/mL is extended to 84 days when stored at 2 – 8℃ plus a further 7 days after being left at room temperature (25℃) for 24 hours. This ensures the unused oxaliplatin infusions are safe to be re-issued to patients, which could reduce drug wastage. The oxalate study suggests that the dose-limiting neurotoxicity of oxaliplatin is unlikely to be directly related to the oxalate produced from oxaliplatin degradation in infusions or from the non-enzymic transformation of oxaliplatin in vivo because the oxalate levels from these routes are minor compared to the endogenous level. The safety and efficacy of dose-banding schemes was demonstrated by comparing the simulated PK characteristics gained from the ex vivo model. Dose-banding with the +10% maximum deviation was selected as the most promising dosing scheme for oxaliplatin. Finally, recommendations are made concerning the introduction of oxaliplatin dose-banding scheme into clinical practice, and on the benefits of harmonised dose-banding schemes.

Subjects/Keywords: 616.99; Oxaliplatin; Dose-banding; Pharmacokinetics; Stability study; Oxalate; Neurotoxicity; Simulation model

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Xiaoqing, L. (2016). Dose-banding studies on oxaliplatin. (Doctoral Dissertation). University of Plymouth. Retrieved from http://hdl.handle.net/10026.1/8081

Chicago Manual of Style (16^th Edition):

Xiaoqing, Liu. “Dose-banding studies on oxaliplatin.” 2016. Doctoral Dissertation, University of Plymouth. Accessed October 19, 2019. http://hdl.handle.net/10026.1/8081.

MLA Handbook (7^th Edition):

Xiaoqing, Liu. “Dose-banding studies on oxaliplatin.” 2016. Web. 19 Oct 2019.

Vancouver:

Xiaoqing L. Dose-banding studies on oxaliplatin. [Internet] [Doctoral dissertation]. University of Plymouth; 2016. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10026.1/8081.

Council of Science Editors:

Xiaoqing L. Dose-banding studies on oxaliplatin. [Doctoral Dissertation]. University of Plymouth; 2016. Available from: http://hdl.handle.net/10026.1/8081

17. Purohit,Anshita R. Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;.

Degree: Zoology, 2015, Gujarat University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/45661

Abstract Not Available

Data not available

Advisors/Committee Members: Rao,M V.

Subjects/Keywords: Antioxidants; Genotoxicity; Mercury; Mitigative; Neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

R, P. (2015). Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;. (Thesis). Gujarat University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/45661

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):

R, Purohit,Anshita. “Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;.” 2015. Thesis, Gujarat University. Accessed October 19, 2019. http://shodhganga.inflibnet.ac.in/handle/10603/45661.

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

MLA Handbook (7^th Edition):

R, Purohit,Anshita. “Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;.” 2015. Web. 19 Oct 2019.

Vancouver:

R P. Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;. [Internet] [Thesis]. Gujarat University; 2015. [cited 2019 Oct 19]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/45661.

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

Council of Science Editors:

R P. Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;. [Thesis]. Gujarat University; 2015. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/45661

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

18. Gopalkrishnan,Avani. Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;.

Degree: Zoology, 2015, Gujarat University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/46371

Abstract Not Available

Data not available

Advisors/Committee Members: Rao,M V.

Subjects/Keywords: Antioxidants; Arsenic; Genotoxicity; Mammals; Neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Gopalkrishnan,Avani. (2015). Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;. (Thesis). Gujarat University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/46371

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

Chicago Manual of Style (16^th Edition):

Gopalkrishnan,Avani. “Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;.” 2015. Thesis, Gujarat University. Accessed October 19, 2019. http://shodhganga.inflibnet.ac.in/handle/10603/46371.

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

MLA Handbook (7^th Edition):

Gopalkrishnan,Avani. “Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;.” 2015. Web. 19 Oct 2019.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

Gopalkrishnan,Avani. Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;. [Internet] [Thesis]. Gujarat University; 2015. [cited 2019 Oct 19]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/46371.

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

Council of Science Editors:

Gopalkrishnan,Avani. Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;. [Thesis]. Gujarat University; 2015. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/46371

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

Temple University

19. Bisen-Hersh, Emily Beth. Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice.

Degree: PhD, 2012, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,190153

►

Psychology

Among children diagnosed with acute lymphoblastic leukemia (ALL) and given chemotherapy-only treatment, 40-70% of survivors experience neurocognitive impairment. Psychostimulants such as methylphenidate are becoming… (more)

▼

Psychology

Among children diagnosed with acute lymphoblastic leukemia (ALL) and given chemotherapy-only treatment, 40-70% of survivors experience neurocognitive impairment. Psychostimulants such as methylphenidate are becoming popular medications for treating these deficits in childhood cancer survivors. However, little is known about the outcome of prescribing stimulants to this population. In the research reported here, a novel preclinical mouse model of ALL treatment was developed and used to investigate the effects of early exposure to methotrexate (MTX) and cytarabine (Ara-C) on learning and memory, and the outcome of treating these deficits using a number of different stimulants. Mouse pups were treated on postnatal day (PND) 14, 15, and 16 with saline, MTX, Ara-C, or two combinations of MTX and Ara-C. At PND 35, significant impairments on learning and memory as measured by autoshaping and novel object recognition were found. Mild deficits were observed in a novel conditional discrimination task, which suggests that extensive training may ameliorate learning impairments. MTX and Ara-C treated mice also exhibited sensitivity to the rewarding and stimulatory properties of amphetamine and methylphenidate, suggesting that typical psychostimulants may become more potent following early chemotherapeutic treatment. In contrast, no increase in drug reward following early exposure to MTX and Ara-C was found for an alternative treatment with possible neuroprotective effects, atomoxetine. These findings were further supported by converging evidence that chemotherapy-treated mice displayed increased novelty-seeking. In addition, a greater percentage of MTX and Ara-C treated mice acquired cocaine self-administration, and maintained a higher number of infusions per session. Overall, these findings highlight the usefulness of preclinical models to examine the developmental effects of early exposure to chemotherapeutic agents on future learning, possible models of cognitive remediation, and the consequences of treating impairments using typical psychostimulant medications.

Temple University – Theses

Advisors/Committee Members: Walker, Ellen A., Hineline, Philip Neil, Marshall, Peter J., Weisberg, Robert W., Gould, Thomas John, Morrison, Mary F. (Mary Frances), Unterwald, Ellen M..

Subjects/Keywords: Psychology; Pharmacology; Neurosciences; Behavioral pharmacology; Chemotherapy; Developmental neurotoxicity; Drug Reward; Learning

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Bisen-Hersh, E. B. (2012). Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,190153

Chicago Manual of Style (16^th Edition):

Bisen-Hersh, Emily Beth. “Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice.” 2012. Doctoral Dissertation, Temple University. Accessed October 19, 2019. http://digital.library.temple.edu/u?/p245801coll10,190153.

MLA Handbook (7^th Edition):

Bisen-Hersh, Emily Beth. “Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice.” 2012. Web. 19 Oct 2019.

Vancouver:

Bisen-Hersh EB. Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Oct 19]. Available from: http://digital.library.temple.edu/u?/p245801coll10,190153.

Council of Science Editors:

Bisen-Hersh EB. Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,190153

Texas A&M University

20. Bellum, Sairam. Neurotoxic mechanisms of methylmercury: cellular and behavior changes.

Degree: 2007, Texas A&M University

URL: http://hdl.handle.net/1969.1/4992

► The organic or methylated form of mercury (Hg), consisting of one methyl group bound to each atom of Hg, (methylmercury; MeHg), accounts for most of… (more)

▼ The organic or methylated form of mercury (Hg), consisting of one methyl group bound to each atom of Hg, (methylmercury; MeHg), accounts for most of the Hg to which humans are exposed. MeHg, by virtue of its lipophilicity is highly neurotoxic to both the developing and mature central nervous system (CNS). Historically, MeHg has been implicated in high morbidity and mortality rates over the last 40 years in Japan, Iraq, Pakistan and Guatemala. The most common symptom exhibited in these exposure episodes was cerebellar ataxia. Recent in vitro studies using cultured granule cells showed that MeHg alters intracellular calcium ion ([Ca2+]i) homeostasis, potentiates reactive oxygen species (ROS) generation and loss of mitochondrial membrane potential leading to apoptotic death of cerebellar granule neurons. To better understand the neurotoxic mechanisms of MeHg on cerebellum, changes with respect to biochemical processes in cerebellar granule cells and associated behavior changes were investigated. The aims of this dissertation were: (1) to assess mercury concentrations in mouse brain using different routes of administration and different tissue preparations, (2) to determine the behavior effects of in vivo MeHg exposure in young adult mice. (3) to understand specific biochemical processes leading to granule cell death/dysfunction due to in vivo MeHg toxicity in mice, and (4) to determine the toxic effects of in vivo MeHg exposure on mice aged between 16-20 months. The present results showed that repeated oral exposure to MeHg results in greater accumulation of Hg in brain tissue when compared to single oral or subcutaneous exposures at the same concentration of MeHg. Behavior analysis revealed that MeHg at the concentrations used in this study had profound effects on motor coordination and balance in young adult and aged mice. Investigation of biochemical processes in cerebellar granule cells of mice exposed to MeHg showed an increase in ROS generation, alteration of ([Ca2+]i (in young adult mice) and loss of MMP in young adult and aged mice. However, these changes did not lead to apoptotic cell death of granule cells at the concentrations of MeHg used and at the specific time point it was investigated in young adult mice. Advisors/Committee Members: Abbott, Louise C (advisor), Donnelly, Kirby C (committee member), Phillips, Timothy D (committee member), Stoica, Gheorghe (committee member).

Subjects/Keywords: Methylmercury; Neurotoxicity; Cerebellum; In vivo

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Bellum, S. (2007). Neurotoxic mechanisms of methylmercury: cellular and behavior changes. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/4992

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):

Bellum, Sairam. “Neurotoxic mechanisms of methylmercury: cellular and behavior changes.” 2007. Thesis, Texas A&M University. Accessed October 19, 2019. http://hdl.handle.net/1969.1/4992.

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

MLA Handbook (7^th Edition):

Bellum, Sairam. “Neurotoxic mechanisms of methylmercury: cellular and behavior changes.” 2007. Web. 19 Oct 2019.

Vancouver:

Bellum S. Neurotoxic mechanisms of methylmercury: cellular and behavior changes. [Internet] [Thesis]. Texas A&M University; 2007. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/1969.1/4992.

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

Council of Science Editors:

Bellum S. Neurotoxic mechanisms of methylmercury: cellular and behavior changes. [Thesis]. Texas A&M University; 2007. Available from: http://hdl.handle.net/1969.1/4992

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

21. Asif, Kunwar. Aluminium phosphide neurotoxicity in albino rat;.

Degree: Chemistry, 1997, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/53793

Abstract available newline newline

Bibliography p. 182-224

Advisors/Committee Members: Nabi, Syed Ashfaq and Riyvi, Shamim Jahan.

Subjects/Keywords: Aluminium; Phosphide; Neurotoxicity; Albino; Rat

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Asif, K. (1997). Aluminium phosphide neurotoxicity in albino rat;. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/53793

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):

Asif, Kunwar. “Aluminium phosphide neurotoxicity in albino rat;.” 1997. Thesis, Aligarh Muslim University. Accessed October 19, 2019. http://shodhganga.inflibnet.ac.in/handle/10603/53793.

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

MLA Handbook (7^th Edition):

Asif, Kunwar. “Aluminium phosphide neurotoxicity in albino rat;.” 1997. Web. 19 Oct 2019.

Vancouver:

Asif K. Aluminium phosphide neurotoxicity in albino rat;. [Internet] [Thesis]. Aligarh Muslim University; 1997. [cited 2019 Oct 19]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/53793.

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

Council of Science Editors:

Asif K. Aluminium phosphide neurotoxicity in albino rat;. [Thesis]. Aligarh Muslim University; 1997. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/53793

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

22. Khan, Farooq. Biochemical studies of glutamate neurotoxicity; -.

Degree: Chemistry, 2000, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/54011

Abstract not available newline newline

Summary p. 188-195

Advisors/Committee Members: Rizvi, Shameem Jahan and Ahmad, Anees.

Subjects/Keywords: Glutamate; Neurotoxicity; Biochemical; Metabolism; Tomatoes

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Khan, F. (2000). Biochemical studies of glutamate neurotoxicity; -. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/54011

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):

Khan, Farooq. “Biochemical studies of glutamate neurotoxicity; -.” 2000. Thesis, Aligarh Muslim University. Accessed October 19, 2019. http://shodhganga.inflibnet.ac.in/handle/10603/54011.

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

MLA Handbook (7^th Edition):

Khan, Farooq. “Biochemical studies of glutamate neurotoxicity; -.” 2000. Web. 19 Oct 2019.

Vancouver:

Khan F. Biochemical studies of glutamate neurotoxicity; -. [Internet] [Thesis]. Aligarh Muslim University; 2000. [cited 2019 Oct 19]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/54011.

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

Council of Science Editors:

Khan F. Biochemical studies of glutamate neurotoxicity; -. [Thesis]. Aligarh Muslim University; 2000. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/54011

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

23. Vadhva, Priti. Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;.

Degree: Zoology, 1989, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/51667

Abstract available newline newline

Bibliography p. 150-166

Advisors/Committee Members: Jafri, A K and Hasan, Mahdi.

Subjects/Keywords: Neurotoxicity; Organophosphorus; Compound; Teleost; Dichlorvos

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Vadhva, P. (1989). Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/51667

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):

Vadhva, Priti. “Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;.” 1989. Thesis, Aligarh Muslim University. Accessed October 19, 2019. http://shodhganga.inflibnet.ac.in/handle/10603/51667.

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

MLA Handbook (7^th Edition):

Vadhva, Priti. “Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;.” 1989. Web. 19 Oct 2019.

Vancouver:

Vadhva P. Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;. [Internet] [Thesis]. Aligarh Muslim University; 1989. [cited 2019 Oct 19]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51667.

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

Council of Science Editors:

Vadhva P. Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;. [Thesis]. Aligarh Muslim University; 1989. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51667

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

University of Cincinnati

24. Bhide, Nirmal S. Tolerance to MDMA-induced serotonergic neurotoxicity.

Degree: PhD, Pharmacy : Pharmaceutical Sciences, 2010, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1267719790

► 3,4-Methylenedioxymethamphetamine (MDMA), an analog of the amphetamine class, is a psychostimulant and a popular drug of abuse. MDMA is considered to be selectively neurotoxic… (more)

▼ 3,4-Methylenedioxymethamphetamine (MDMA), an analog of the amphetamine class, is a psychostimulant and a popular drug of abuse. MDMA is considered to be selectively neurotoxic to serotonergic nerve terminals in different brain regions. Repeated exposure to MDMA during adolescence is neuroprotective against a subsequent neurotoxic regimen of MDMA in adulthood. This phenomenon is similar to ischemic preconditioning, where repeated exposure to sub-lethal insults results in neuroprotection against a subsequent deleterious insult. The purpose of this study was to evaluate whether repeated exposure (preconditioning) to a non-toxic dose of MDMA in adult rats provides neuroprotection against subsequent MDMA induced 5-HT depletion and to evaluate the mechanisms involved. Preconditioning with MDMA (10 mg/kg i.p.) daily for 4 days provided significant protection against MDMA-induced 5-HT depletion in the striatum, hippocampus and cortex. Preconditioning with MDMA (10 mg/kg i.p.) daily for 4 days provided significant protection against methamphetamine (METH)-induced 5-HT, but not DA, depletion in the striatum. Since the neuroprotection is specific to the serotonergic neurons, it is possible that preconditioning with MDMA results in neuroadaptive changes in 5-HT containing neurons. The role for alterations in MDMA-induced hyperthermia and brain MDMA concentrations was ruled out. Repeated exposure to Clozapine, at doses known to produce 5-HT2 receptor downregulation, provided significant protection against MDMA-induced 5-HT depletion in the striatum, hippocampus and cortex. However, it is inconclusive whether repeated exposure to MDMA results in downregulation of 5-HT2 receptor function and expression. Repeated exposure to MDMA resulted in the downregulation of serotonin transporter (SERT) expression. Steady state 5-HT uptake in hippocampal synaptosomal preparations in rats previously exposed to MDMA was significantly reduced when compared to vehicle treated animals. SERT plays a key role in MDMA-induced 5-HT neurotoxicity and downregulation of SERT function after preconditioning with MDMA may contribute towards the neuroprotection. Taken together, these studies suggest that repeated exposure to MDMA provides protection against a 5-HT depleting dose of MDMA and that downregulation of SERT function may contribute towards this neuroprotective phenomenon. Advisors/Committee Members: Gudelsky, Gary (Committee Chair).

Subjects/Keywords: Pharmacology; MDMA; Serotonin; preconditioning; tolerance; neurotoxicity; serotonin transporter

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Bhide, N. S. (2010). Tolerance to MDMA-induced serotonergic neurotoxicity. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1267719790

Chicago Manual of Style (16^th Edition):

Bhide, Nirmal S. “Tolerance to MDMA-induced serotonergic neurotoxicity.” 2010. Doctoral Dissertation, University of Cincinnati. Accessed October 19, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1267719790.

MLA Handbook (7^th Edition):

Bhide, Nirmal S. “Tolerance to MDMA-induced serotonergic neurotoxicity.” 2010. Web. 19 Oct 2019.

Vancouver:

Bhide NS. Tolerance to MDMA-induced serotonergic neurotoxicity. [Internet] [Doctoral dissertation]. University of Cincinnati; 2010. [cited 2019 Oct 19]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1267719790.

Council of Science Editors:

Bhide NS. Tolerance to MDMA-induced serotonergic neurotoxicity. [Doctoral Dissertation]. University of Cincinnati; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1267719790

NSYSU

25. Li, Yu-Ru. To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.

Degree: Master, Biological Sciences, 2016, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

► Alzheimer's disease (AD) is one of the common form of age-related neurodegenerative diseases and the leading cause of senile dementia. In the beta-amyloid (AÎ²) cascade… (more)

Subjects/Keywords: Î²-amyloid; Amyloid precursor protein; Alzheimer's disease; DNA repair; Neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Li, Y. (2016). To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

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):

Li, Yu-Ru. “To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.” 2016. Thesis, NSYSU. Accessed October 19, 2019. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537.

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

MLA Handbook (7^th Edition):

Li, Yu-Ru. “To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.” 2016. Web. 19 Oct 2019.

Vancouver:

Li Y. To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. [Internet] [Thesis]. NSYSU; 2016. [cited 2019 Oct 19]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537.

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

Council of Science Editors:

Li Y. To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. [Thesis]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

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

University of Louisville

26. Potts, Lisa Fryman. Annonacin in Asimina triloba fruit : implications for neurotoxicity.

Degree: PhD, 2011, University of Louisville

URL: 10.18297/etd/1145 ; https://ir.library.louisville.edu/etd/1145

► The acetogenin annonacin, from the tropical annonaceous plant Annona muricata, is a lipophilic, mitochondrial complex I inhibitor reported to be more toxic than rotenone to… (more)

▼ The acetogenin annonacin, from the tropical annonaceous plant Annona muricata, is a lipophilic, mitochondrial complex I inhibitor reported to be more toxic than rotenone to mesencephalic neurons. The temperate annonaceous plant Asimina tri/oba (pawpaw) is native to the Eastern United States and its products are available online. This study determined whether annonacin is in the pawpaw fruit pulp and whether it or the crude ethyl acetate (EtOAc) extract is toxic to cortical neurons and induces pathological changes in the microtubule associated protein tau. Pawpaw extract was prepared by pulp extraction with methanol and liquid-liquid partitioning with EtOAc. Annonacin was isolated from the crude EtOAc extract via column chromatography using a gradient solvent system of increasing polarity. Mass spectroscopy, nuclear magnetic resonance and infrared spectroscopy were used to compare isolated material with synthetic annonacin and a natural annonacin sample. Toxicity of isolated annonacin and the total EtOAc extract were determined in primary rat cortical neurons using the MIT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. The effects of annonacin on tau phosphorylation were determined by immunocytochemistry and western blot analysis. The average concentration of annonacin in the fruit pulp was 0.07 ± 0.03 mg/g. Purified annonacin (30.07 µg/ml) and crude EtOAc extract (47.96 µg/ml) reduced relative viability of cortical neurons by 50% 48 hours post treatment. Annonacin toxicity was enhanced in the presence of crude extract. Annonacin treatment resulted in a decrease in the neuronal specific marker microtubule associated protein 2 (MAP2) and tau immunoreactivity, and tau expression was decreased on western blot. In conclusion, Asimina triloba fruit contains a high concentration of annonacin, which is toxic to cortical neurons. Based on these results, annonacin acts to reduce overall levels of tau, though it remains elusive whether or not this is a direct or indirect effect of annonacin action. Crude fruit extract also induced neurotoxicity, highlighting the need for additional studies to determine the bioavailability after consumption and potential risks of neurodegeneration associated with chronic exposure to pawpaw products. Advisors/Committee Members: Litvan, Irene.

Subjects/Keywords: Annonacin; Pawpaw; Asimina triloba; Annonaceous acetogenins; Tau; Neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Potts, L. F. (2011). Annonacin in Asimina triloba fruit : implications for neurotoxicity. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/1145 ; https://ir.library.louisville.edu/etd/1145

Chicago Manual of Style (16^th Edition):

Potts, Lisa Fryman. “Annonacin in Asimina triloba fruit : implications for neurotoxicity.” 2011. Doctoral Dissertation, University of Louisville. Accessed October 19, 2019. 10.18297/etd/1145 ; https://ir.library.louisville.edu/etd/1145.

MLA Handbook (7^th Edition):

Potts, Lisa Fryman. “Annonacin in Asimina triloba fruit : implications for neurotoxicity.” 2011. Web. 19 Oct 2019.

Vancouver:

Potts LF. Annonacin in Asimina triloba fruit : implications for neurotoxicity. [Internet] [Doctoral dissertation]. University of Louisville; 2011. [cited 2019 Oct 19]. Available from: 10.18297/etd/1145 ; https://ir.library.louisville.edu/etd/1145.

Council of Science Editors:

Potts LF. Annonacin in Asimina triloba fruit : implications for neurotoxicity. [Doctoral Dissertation]. University of Louisville; 2011. Available from: 10.18297/etd/1145 ; https://ir.library.louisville.edu/etd/1145

University of California – Berkeley

27. Lantz, Stephen R. Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon.

Degree: Molecular Toxicology, 2013, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/7mr2s4s4

► Organophosphorus (OP) compounds have found tremendous use as industrial chemicals, pharmaceuticals and chemical warfare agents. The intended toxicity of warfare agents and the unwanted toxicity… (more)

▼ Organophosphorus (OP) compounds have found tremendous use as industrial chemicals, pharmaceuticals and chemical warfare agents. The intended toxicity of warfare agents and the unwanted toxicity of industrial and agrochemicals results primarily from inhibition of cholinesterase enzymes, predominantly acetylcholinesterase (AChE). Functionalization of the OP class has led to development of compounds with selective action at various primary protein targets and the identification of numerous secondary and tertiary off target effects. Two OP compounds, glufosinate (GLF) and ethephon, have significant agricultural use as an herbicide and plant growth regulator respectively. They are also characterized by atypical mammalian OP toxicity. This dissertation explores newly characterized aspects of GLF and ethephon mammalian toxicology.GLF can cause convulsions in mammals without AChE inhibition. The structural similarity of GLF to glutamate and the known excitatory mechanisms of glutamate signaling implicate the glutamatergic system as a target for GLF neurotoxicity. Known glutamate targets which could reasonably be expected to be involved in a convulsive phenotype after modulation were assayed for effect by GLF and related compounds. There appears to be no effect of GLF or the primary metabolite N-acetyl-GLF (N-Ac-GLF) on the urea cycle regulator enzyme CPS-I. However, GLF and N-Ac-GLF can interact directly with the N-methyl-D-aspartate (NMDA) subtype glutamate receptor and the high affinity glutamate reuptake transporter GLT-I. Potency at the NMDAR is in the range of 10-10,000 μM and potency at GLT-I is >1,000 μM. The concentrations required to affect transport through GLT-I are likely not to be attained and therefore not relevant to the neurotoxic mode of action. However, toxicokinetic data from reports of intentional human poisonings suggest that the concentration of GLF in the brain could reach high enough levels after acute exposure to account for the convulsive and memory loss effects. Furthermore, the newly characterized action of N-Ac-GLF at the NMDAR suggests that both the parent compound and metabolite could contribute to neurotoxicity.Direct radioligand binding experiments are one of the most unbiased approaches to target site identification. However, the preparation of high specific activity radioligands for compounds of interest is specialized and costly. Progress toward the preparation of [³H-Me] GLF is reported with successful synthesis of unlabeled GLF prepared with methyl addition and deprotection as the last synthetic step. Although the synthetic procedure was not scalable for economical radiosynthesis, the method provides a platform for further optimization and eventual radioligand synthesis.Ethephon is well characterized to readily degrade to ethylene, which acts as a regulator of plant growth. Butyrylcholinesterase (BChE) is selectively inhibited after exposure to ethephon. Ethephon…

Subjects/Keywords: Toxicology; Analytical chemistry; Neurosciences; butyrylcholinesterase; ethephon; glufosinate; herbicides; neurotoxicity; NMDA receptor

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lantz, S. R. (2013). Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/7mr2s4s4

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):

Lantz, Stephen R. “Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon.” 2013. Thesis, University of California – Berkeley. Accessed October 19, 2019. http://www.escholarship.org/uc/item/7mr2s4s4.

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

MLA Handbook (7^th Edition):

Lantz, Stephen R. “Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon.” 2013. Web. 19 Oct 2019.

Vancouver:

Lantz SR. Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon. [Internet] [Thesis]. University of California – Berkeley; 2013. [cited 2019 Oct 19]. Available from: http://www.escholarship.org/uc/item/7mr2s4s4.

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

Council of Science Editors:

Lantz SR. Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon. [Thesis]. University of California – Berkeley; 2013. Available from: http://www.escholarship.org/uc/item/7mr2s4s4

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

Duke University

28. Gonzalez-Hunt, Claudia Patricia. Toxicant-Induced Mitochondrial Dysfunction and Dopaminergic Neurodegeneration in Caenorhabditis elegans .

Degree: 2017, Duke University

URL: http://hdl.handle.net/10161/14382

► Mitochondrial dysfunction appears to be a hallmark of many neurodegenerative diseases. The link between mitochondrial and neuronal health is particularly strong in Parkinson’s disease… (more)

▼ Mitochondrial dysfunction appears to be a hallmark of many neurodegenerative diseases. The link between mitochondrial and neuronal health is particularly strong in Parkinson’s disease (PD). Genes that have been shown to cause PD when mutated are known to interact with mitochondria to varying degrees; particularly, two of the genes associated with mitochondria-specific autophagy (mitophagy), PINK1 and PARK2, have been shown to cause autosomal recessive PD. Deletions and mutations in mitochondrial DNA (mtDNA) have been detected in the substantia nigra of PD patients. Furthermore, toxicants used to model PD in the laboratory are known to exert their toxicity by disrupting mitochondrial function. Despite all the advances in PD research, the precise mechanisms through which this disease arises are still not well understood. The central goal of this dissertation was to investigate the role that mtDNA damage and mitochondrial dysfunction play in causing dopaminergic neurodegeneration in the context of PD. This work was performed with a particular focus on mitochondrial toxicants: their mechanism of action and effect on neuronal health, and how these toxic exposures might exacerbate genetic susceptibilities. Another goal was to identify windows of susceptibility to mtDNA damage, with early life and old age being of particular interest. To explore these ideas, the nematode Caenorhabditis elegans was utilized as a model organism. To characterize age-related sensitivity to mtDNA damage, worms at different life stages were exposed to ultraviolet C (UVC) to accumulate mtDNA damage and the effect of this damage on mitochondrial genome copy number and dopaminergic neuron health was assessed. To evaluate the role of autophagy in maintaining mitochondrial and neuronal health after toxicant exposure, mitophagy gene knockouts (KOs) and wild type worms were exposed to 6-hydroxydopamine (6-OHDA) and UVC; to study non-selective macroautophagy, starvation was used to induce it, and nematodes were subsequently subjected to a toxic exposure. Dopaminergic neuron morphology, targeted gene expression, and mitochondrial morphology were evaluated. Lastly, the mechanism of toxicity of rotenone in C. elegans was investigated; specifically, mitochondrial respiration (with the Seahorse Bioanalyzer), targeted metabolomics, ATP levels, and targeted gene expression were evaluated. Due to technical complications with our UVC exposure model and PCR-based evaluation of mtDNA damage in C. elegans eggs, the windows of susceptibility to mtDNA damage hypothesis could not be properly tested. However, our current results do not support this idea. Our studies on the role of autophagy in the context of toxicant-induced dopaminergic neurodegeneration suggest that both non-selective macroautophagy and mitophagy have a protective effect. We saw protection from 6-OHDA-induced neurodegeneration after starvation treatment, suggesting that macroautophagy could be playing a protective role. In the context of mitophagy mutations, we saw different… Advisors/Committee Members: Meyer, Joel N (advisor).

Subjects/Keywords: Toxicology; Environmental health; Neurosciences; Caenorhabditis elegans; genotoxicity; mitochondria; mitophagy; neurodegeneration; neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Gonzalez-Hunt, C. P. (2017). Toxicant-Induced Mitochondrial Dysfunction and Dopaminergic Neurodegeneration in Caenorhabditis elegans . (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/14382

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):

Gonzalez-Hunt, Claudia Patricia. “Toxicant-Induced Mitochondrial Dysfunction and Dopaminergic Neurodegeneration in Caenorhabditis elegans .” 2017. Thesis, Duke University. Accessed October 19, 2019. http://hdl.handle.net/10161/14382.

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

MLA Handbook (7^th Edition):

Gonzalez-Hunt, Claudia Patricia. “Toxicant-Induced Mitochondrial Dysfunction and Dopaminergic Neurodegeneration in Caenorhabditis elegans .” 2017. Web. 19 Oct 2019.

Vancouver:

Gonzalez-Hunt CP. Toxicant-Induced Mitochondrial Dysfunction and Dopaminergic Neurodegeneration in Caenorhabditis elegans . [Internet] [Thesis]. Duke University; 2017. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10161/14382.

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

Council of Science Editors:

Gonzalez-Hunt CP. Toxicant-Induced Mitochondrial Dysfunction and Dopaminergic Neurodegeneration in Caenorhabditis elegans . [Thesis]. Duke University; 2017. Available from: http://hdl.handle.net/10161/14382

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

Virginia Tech

29. Balbuena, Pergentino. Neurotoxic effects of malathion and lead acetate on the blood-brain barrier: Disruptive effects caused by different mechanisms examined with an in vitro blood-brain barrier system.

Degree: PhD, Biomedical and Veterinary Sciences, 2010, Virginia Tech

URL: http://hdl.handle.net/10919/77115

► Organophosphates (OP) such as malathion are organic derivatives of phosphoric acid with broad use in everyday life throughout the world, especially as insecticides. Lead particles… (more)

▼ Organophosphates (OP) such as malathion are organic derivatives of phosphoric acid with broad use in everyday life throughout the world, especially as insecticides. Lead particles can accumulate in soil and from there leach into our water supplies. Interaction with the environment offers opportunities for multiple exposures to combinations of different toxicants (such as lead and malathion). Thus, it is important to assess effects that these compounds exert not only on the nervous system, but also on the blood-brain barrier (BBB). The BBB consists of specialized endothelial cells that form the vasculature of the brain; it regulates passage of nutrients, while preventing potentially damaging substances from entering the brain. The main feature of the BBB is the presence of tight junctions between cells, which provide the BBB with its low permeability. The work presented in this dissertation tests the hypothesis that lead and malathion disrupt BBB integrity by affecting tight junctions of the BBB. The hypothesis suggests that disruptions involve changes in protein levels and gene expression as well as activation of transient receptor potential canonical channels (TRPC) that in turn increase intracellular calcium levels affecting tight junction structure. The hypothesis was tested by assessing lead-malathion interactions in an in vitro BBB model. This model was constructed with rat astrocytes and rat brain endothelial cells (RBE4). Assessments of cell toxicity in response to different concentrations of the neurotoxicants tested showed that concentrations between 10-5 µM and 10-6 µM were ideal to assess combinations of neurotoxicants. In general, protein levels of occludin, claudin 5, ZO1, and ZO2 decreased at all times, however, qPCR analysis of gene expression for all the proteins did not correlate with the assessments on protein levels. TRPC channel protein levels increased in response to neurotoxicant insult, which correlated with results for gene expression. This study suggests that at least one of the mechanisms that neurotoxicants lead and malathion utilize to disrupt permeability of the BBB is by affecting tight junction structure. This effect could be regulated by increases in gene expression of TRPC1 and TRPC4 that are associated with increases in the number of TRPC channels on the membrane of endothelial cells of the cerebral microvasculature. Advisors/Committee Members: Ehrich, Marion F. (committeechair), Lee, Yong Woo (committee member), Eyre, Peter (committee member), Jortner, Bernard S. (committee member), Meldrum, James Blair (committee member).

Subjects/Keywords: blood-brain barrier; Malaoxon; Malathion; Lead acetate; neurotoxicity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Balbuena, P. (2010). Neurotoxic effects of malathion and lead acetate on the blood-brain barrier: Disruptive effects caused by different mechanisms examined with an in vitro blood-brain barrier system. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/77115

Chicago Manual of Style (16^th Edition):

Balbuena, Pergentino. “Neurotoxic effects of malathion and lead acetate on the blood-brain barrier: Disruptive effects caused by different mechanisms examined with an in vitro blood-brain barrier system.” 2010. Doctoral Dissertation, Virginia Tech. Accessed October 19, 2019. http://hdl.handle.net/10919/77115.

MLA Handbook (7^th Edition):

Balbuena, Pergentino. “Neurotoxic effects of malathion and lead acetate on the blood-brain barrier: Disruptive effects caused by different mechanisms examined with an in vitro blood-brain barrier system.” 2010. Web. 19 Oct 2019.

Vancouver:

Balbuena P. Neurotoxic effects of malathion and lead acetate on the blood-brain barrier: Disruptive effects caused by different mechanisms examined with an in vitro blood-brain barrier system. [Internet] [Doctoral dissertation]. Virginia Tech; 2010. [cited 2019 Oct 19]. Available from: http://hdl.handle.net/10919/77115.

Council of Science Editors:

Balbuena P. Neurotoxic effects of malathion and lead acetate on the blood-brain barrier: Disruptive effects caused by different mechanisms examined with an in vitro blood-brain barrier system. [Doctoral Dissertation]. Virginia Tech; 2010. Available from: http://hdl.handle.net/10919/77115

University of South Florida

30. Grimmig, Beth. Astaxanthin Attenuates MPTP Induced Neurotoxicity and Modulates Cognitive Function in Aged Mice.

Degree: 2017, University of South Florida

URL: https://scholarcommons.usf.edu/etd/7405

► Parkinson’s disease is the second common neurodegenerative disease and is most frequently diagnosed in individuals over 60. There are no available medications that can prevent… (more)

Subjects/Keywords: Astaxanthin; Neuroprotection; Neurotoxicity; Neurodegeneration; MPTP; Aging; Cognition; Neurosciences

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Grimmig, B. (2017). Astaxanthin Attenuates MPTP Induced Neurotoxicity and Modulates Cognitive Function in Aged Mice. (Thesis). University of South Florida. Retrieved from https://scholarcommons.usf.edu/etd/7405

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):

Grimmig, Beth. “Astaxanthin Attenuates MPTP Induced Neurotoxicity and Modulates Cognitive Function in Aged Mice.” 2017. Thesis, University of South Florida. Accessed October 19, 2019. https://scholarcommons.usf.edu/etd/7405.

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

MLA Handbook (7^th Edition):

Grimmig, Beth. “Astaxanthin Attenuates MPTP Induced Neurotoxicity and Modulates Cognitive Function in Aged Mice.” 2017. Web. 19 Oct 2019.

Vancouver:

Grimmig B. Astaxanthin Attenuates MPTP Induced Neurotoxicity and Modulates Cognitive Function in Aged Mice. [Internet] [Thesis]. University of South Florida; 2017. [cited 2019 Oct 19]. Available from: https://scholarcommons.usf.edu/etd/7405.

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

Council of Science Editors:

Grimmig B. Astaxanthin Attenuates MPTP Induced Neurotoxicity and Modulates Cognitive Function in Aged Mice. [Thesis]. University of South Florida; 2017. Available from: https://scholarcommons.usf.edu/etd/7405

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

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations