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Exposure to paraquat results in Parkinson\u2019s disease (PD)-like symptoms including dopaminergic cell loss. Nutrition has also been linked in the pathogenesis of PD, such as reduced levels of folic acid, a B-vitamin, and component of one-carbon metabolism. Within one-carbon metabolism, methylenetetrahydrofolate reductase (MTHFR) catalyzes the irreversible conversion of 5, 10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. A polymorphism in MTHFR (677\u2009C&amp;\u2192T) has been reported in 5%\u201315% of North American and European human populations. The MTHFR polymorphism is also prevalent in PD patients. The goal of this study was to investigate the impact of paraquat-induced PD-like pathology in the context of reduced levels of MTHFR. Three-month-old male Mthfr+\/\u2212 mice, which model the MTHFR polymorphism observed in humans, were administered intraperitoneal injections of paraquat (10 mg\/kg) or saline 6 times over 3 weeks. At the end of paraquat treatment, motor and memory function were assessed followed by collection of brain tissue for biochemical analysis. Mthfr+\/\u2013 mice treated with paraquat showed impaired motor function. There was increased microglial activation within the substantia nigra (SN) of Mthfr+\/\u2212 mice treated with paraquat. Additionally, all Mthfr+\/\u2212 mice that were treated with paraquat showed increased oxidative stress within the dorsal striatum, but not the SN. The present results show that paraquat exposure increases PD-like pathology in mice deficient in one-carbon metabolism.<\/jats:p>","DOI":"10.1093\/toxsci\/kfz034","type":"journal-article","created":{"date-parts":[[2019,2,5]],"date-time":"2019-02-05T20:42:44Z","timestamp":1549399364000},"page":"25-33","source":"Crossref","is-referenced-by-count":13,"title":["Paraquat Exposure Increases Oxidative Stress Within the Dorsal Striatum of Male Mice With a Genetic Deficiency in One-carbon Metabolism"],"prefix":"10.1093","volume":"169","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3557-7307","authenticated-orcid":false,"given":"Nafisa M","family":"Jadavji","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lauren K","family":"Murray","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joshua T","family":"Emmerson","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chris A","family":"Rudyk","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shawn","family":"Hayley","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patrice D","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Carleton University, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2019,2,6]]},"reference":[{"key":"2020071623370378000_kfz034-B1","doi-asserted-by":"crossref","first-page":"12","DOI":"10.1016\/j.brainresbull.2017.03.009","article-title":"Metabolic dysfunction in Parkinson\u2019s disease: Bioenergetics, redox homeostasis and central carbon metabolism","volume":"133","author":"Anandhan","year":"2017","journal-title":"Brain Res. 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