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dc.contributor.advisorSun, Albert Y.eng
dc.contributor.authorMiller, Rebecca Louise, 1974-eng
dc.date.issued2007eng
dc.date.submitted2007 Springeng
dc.description"May 2007"eng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionVita.eng
dc.descriptionThesis (Ph. D.) University of Missouri-Columbia 2007.eng
dc.description.abstractParkinson's disease (PD) is a neurodegenerative disorder known to affect the dopaminergic neurons in the substantia nigra. Epidemiological studies have shown an increased risk of developing PD with exposure to paraquat. In this study, we examined the source of reactive oxygen species (ROS) and the underlying signaling pathway for paraquat-induced cytotoxicity to BV-2 microglial cells. Paraquat-induced ROS production was attenuate by inhibitors for NADPH oxidase, protein kinase C and extracellular signal-regulated kinases 1/2. Under inflammatory conditions, microglial cells respond to cytokines by induction of inducible nitric oxide synthase which produces nitric oxide (NO). Our results show that paraquat inhibited cytokine-induced NO production but only moderately enhanced ROS production in microglial cells. We wanted to determine the role of NADPH oxidase in neuronal cells. Paraquat induced the upregulation of the p67phox subunit protein and NOX2 mRNA of NADPH oxidase in differentiated SH-SY5Y cells. In conclusion, our data suggest that NADPH oxidase plays a significant role in the toxicity of paraquat.eng
dc.description.bibrefIncludes bibliographical referenceseng
dc.identifier.merlinb6666200xeng
dc.identifier.oclc316508115eng
dc.identifier.urihttps://doi.org/10.32469/10355/4764eng
dc.identifier.urihttps://hdl.handle.net/10355/4764
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.rightsOpenAccess.eng
dc.rights.licenseThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.
dc.subject.meshReactive Oxygen Species -- metabolismeng
dc.subject.meshParkinson Disease -- etiologyeng
dc.subject.meshNADPH Oxidase -- drug effectseng
dc.subject.meshNerve Degeneration -- chemically inducedeng
dc.subject.meshMicroglia -- drug effectseng
dc.subject.meshParaquat -- toxicityeng
dc.titleThe mechanism for paraquat toxicity involves oxidative stress and inflammation : a model for Parkinson's diseaseeng
dc.typeThesiseng
thesis.degree.disciplinePharmacology (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


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