{"id":{"repo_id":"missouri","oai_identifier":"oai:mospace.umsystem.edu:10355/4764"},"canonical_url":"https://search.dev.ndltd.org/etd/missouri/oai:mospace.umsystem.edu:10355/4764","repository":{"repo_id":"missouri","name":"University of Missouri","base_url":"https://mospace.umsystem.edu/oai/request"},"display":{"title":"The mechanism for paraquat toxicity involves oxidative stress and inflammation : a model for Parkinson's disease","abstract":"Parkinson'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.","abstract_html":"Parkinson'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.","abstract_has_math":false,"creators":["Miller, Rebecca Louise, 1974-"],"institution":"University of Missouri--Columbia","degree_name":"Ph. D.","degree_level":"Doctoral","degree_discipline":"Medical pharmacology and physiology (MU)","degree_department":null,"school":null,"contributors":[],"advisors":["Sun, Albert Y."],"committee_chairs":[],"committee_members":[],"year":2007,"date_issued":"2007","date_published":"2007","updated_at":"2026-07-24T03:08:54Z","subjects":[],"languages":["eng","English"],"rights":["OpenAccess."],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.32469/10355/4764"],"render_values":[{"text":"https://doi.org/10.32469/10355/4764","href":"https://doi.org/10.32469/10355/4764","code":true}]}]},"links":{"outbound_url":"https://hdl.handle.net/10355/4764","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Sun, Albert Y."]},{"key":"dc:creator","label":"Author","values":["Miller, Rebecca Louise, 1974-"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2010-01-12T18:42:00Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2010-01-12T18:42:00Z"]},{"key":"dc:date.issued","label":"Date","values":["2007"]},{"key":"dc:publisher","label":"Institution","values":["University of Missouri--Columbia"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Medical pharmacology and physiology (MU)"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph. D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Missouri--Columbia"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["English"]},{"key":"dc:language.iso","label":"Language (ISO)","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["OpenAccess."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.32469/10355/4764"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/10355/4764"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["\"May 2007\"","The 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.","Vita.","Thesis (Ph. D.) University of Missouri-Columbia 2007."]},{"key":"dc:description.abstract","label":"Abstract","values":["Parkinson'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."]},{"key":"dc:title","label":"Title","values":["The mechanism for paraquat toxicity involves oxidative stress and inflammation : a model for Parkinson's disease"]}]}],"canonical_facts":{"dc:contributor.advisor":["Sun, Albert Y."],"dc:creator":["Miller, Rebecca Louise, 1974-"],"dc:date.accessioned":["2010-01-12T18:42:00Z"],"dc:date.available":["2010-01-12T18:42:00Z"],"dc:date.issued":["2007"],"dc:description":["\"May 2007\"","The 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.","Vita.","Thesis (Ph. D.) University of Missouri-Columbia 2007."],"dc:description.abstract":["Parkinson'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."],"dc:identifier.doi":["https://doi.org/10.32469/10355/4764"],"dc:identifier.uri":["https://hdl.handle.net/10355/4764"],"dc:language":["English"],"dc:language.iso":["eng"],"dc:publisher":["University of Missouri--Columbia"],"dc:rights":["OpenAccess."],"dc:title":["The mechanism for paraquat toxicity involves oxidative stress and inflammation : a model for Parkinson's disease"],"dc:type":["Thesis"],"thesis:degree_discipline":["Medical pharmacology and physiology (MU)"],"thesis:degree_level":["Doctoral"],"thesis:degree_name":["Ph. D."],"thesis:institution_name":["University of Missouri--Columbia"]},"updated_at":"2026-07-24T03:08:54Z"}