{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T08:17:06Z","timestamp":1791101826511,"version":"4.1.0"},"reference-count":75,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2012,10,8]],"date-time":"2012-10-08T00:00:00Z","timestamp":1349654400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2012,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Paraquat is one of the most widely used herbicides worldwide. It produces a Parkinson's disease (PD) model in rodents through redox cycling and oxidative stress (OS) and is associated with PD risk in humans. Glutathione transferases provide cellular protection against OS and could potentially modulate paraquat toxicity. We investigated PD risk associated with paraquat use in individuals with homozygous deletions of the genes encoding glutathione <jats:italic>S<\/jats:italic>\u2010transferase M1 (GSTM1) or T1 (GSTT1). Eighty\u2010seven PD subjects and 343 matched controls were recruited from the Agricultural Health Study, a study of licensed pesticide applicators and spouses in Iowa and North Carolina. PD was confirmed by in\u2010person examination. Paraquat use and covariates were determined by interview. We genotyped subjects for homozygous deletions of <jats:italic>GSTM1<\/jats:italic> (<jats:italic>GSTM1*0<\/jats:italic>) and <jats:italic>GSTT1<\/jats:italic> (<jats:italic>GSTT1*0<\/jats:italic>) and tested interaction between paraquat use and genotype using logistic regression. Two hundred and twenty\u2010three (52%) subjects had <jats:italic>GSTM1*0<\/jats:italic>, 95 (22%) had <jats:italic>GSTT1*0<\/jats:italic>, and 73 (17%; all men) used paraquat. After adjustment for potential confounders, there was no interaction with <jats:italic>GSTM1<\/jats:italic>. In contrast, <jats:italic>GSTT1<\/jats:italic> genotype significantly modified the association between paraquat and PD. In men with functional <jats:italic>GSTT1<\/jats:italic>, the odds ratio (OR) for association of PD with paraquat use was 1.5 (95% confidence interval [CI]: 0.6\u20133.6); in men with <jats:italic>GSTT1*0<\/jats:italic>, the OR was 11.1 (95% CI: 3.0\u201344.6; <jats:italic>P<\/jats:italic> interaction: 0.027). Although replication is needed, our results suggest that PD risk from paraquat exposure might be particularly high in individuals lacking GSTT1. <jats:italic>GSTT1*0<\/jats:italic> is common and could potentially identify a large subpopulation at high risk of PD from oxidative stressors such as paraquat. \u00a9 2012 <jats:italic>Movement<\/jats:italic> Disorder Society<\/jats:p>","DOI":"10.1002\/mds.25216","type":"journal-article","created":{"date-parts":[[2012,10,8]],"date-time":"2012-10-08T12:12:14Z","timestamp":1349698334000},"page":"1652-1658","source":"Crossref","is-referenced-by-count":85,"title":["Genetic modification of the association of paraquat and Parkinson's disease"],"prefix":"10.1002","volume":"27","author":[{"given":"Samuel M.","family":"Goldman","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Freya","family":"Kamel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. 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William","family":"Langston","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline M.","family":"Tanner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,10,8]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.10483"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbagen.2008.02.005"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1427.023"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2165"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/ncpneuro0924"},{"key":"e_1_2_7_7_2","first-page":"387","volume-title":"Parkinson's Disease: Diagnosis and Clinical Management","author":"Tanner CM","year":"2008"},{"key":"e_1_2_7_8_2","first-page":"435","article-title":"A meta\u2010analysis of Parkinson's disease and exposure to pesticides","volume":"21","author":"Priyadarshi A","year":"2000","journal-title":"Neurotoxicology"},{"key":"e_1_2_7_9_2","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.8095"},{"key":"e_1_2_7_10_2","doi-asserted-by":"publisher","DOI":"10.1289\/ehp.1002839"},{"key":"e_1_2_7_11_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C100560200"},{"key":"e_1_2_7_12_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2005.03088.x"},{"key":"e_1_2_7_13_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1460-9568.2005.04301.x"},{"key":"e_1_2_7_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1383-5742(00)00050-8"},{"key":"e_1_2_7_15_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.pharmtox.45.120403.095857"},{"key":"e_1_2_7_16_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj3240025"},{"key":"e_1_2_7_17_2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.2000.3087"},{"key":"e_1_2_7_18_2","first-page":"21","article-title":"Purification, characterization, and tissue distribution of human class theta glutathione S\u2010transferase T1\u20101","volume":"39","author":"Juronen E","year":"1996","journal-title":"Biochem Mol Biol Int"},{"key":"e_1_2_7_19_2","first-page":"1199","article-title":"Expression of glutathione S\u2010transferase T1 (GSTT1) in human brain tumours","volume":"21","author":"Diedrich A","year":"2006","journal-title":"Histol Histopathol"},{"key":"e_1_2_7_20_2","first-page":"4920","article-title":"Effects of human and rat glutathione S\u2010transferases on the covalent DNA binding of the N\u2010acetoxy derivatives of heterocyclic amine carcinogens in vitro: a possible mechanism of organ specificity in their carcinogenesis","volume":"54","author":"Lin D","year":"1994","journal-title":"Cancer Res"},{"key":"e_1_2_7_21_2","first-page":"271","article-title":"Enzymes and transport systems involved in the formation and disposition of glutathione S\u2010conjugates","volume":"47","author":"Commandeur JN","year":"1995","journal-title":"Role in bioactivation and detoxication mechanisms of xenobiotics. 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