MovDisordV3, Main, Exploration, bibRecord, 001110

Genetic Modification of the Association of Paraquat and Parkinson's Disease

Identifieur interne : 001110 ( Main/Exploration ); précédent : 001109; suivant : 001111

Genetic Modification of the Association of Paraquat and Parkinson's Disease

Auteurs : Samuel M. Goldman [États-Unis] ; Freya Kamel [États-Unis] ; G. Webster Ross [États-Unis] ; Grace S. Bhudhikanok [États-Unis] ; Jane A. Hoppin [États-Unis] ; Monica Korell [États-Unis] ; Connie Marras [Canada] ; Cheryl Meng [États-Unis] ; David M. Umbach [États-Unis] ; Meike Kasten [Allemagne] ; Anabel R. Chade [Argentine] ; Kathleen Comyns [États-Unis] ; Marie B. Richards [États-Unis] ; Dale P. Sandler [États-Unis] ; Aaron Blair [États-Unis] ; J. William Langston [États-Unis] ; Caroline M. Tanner [États-Unis]

Source :

Movement disorders [ 0885-3185 ] ; 2012.

RBID : Pascal:13-0017931

Descripteurs français

Pascal (Inist)
- Maladie de Parkinson, Pathologie du système nerveux, Modification, Glutathione transferase, Pesticide, Environnement, Interaction.
Wicri :
- topic : Pesticide.

English descriptors

KwdEn :
- Age Factors, Aged, Aged, 80 and over, Case-Control Studies, Cohort Studies, Diagnosis, Computer-Assisted, Disease Susceptibility (chemically induced), Disease Susceptibility (epidemiology), Environment, Female, Gene Deletion, Genetic Association Studies, Genotype, Glutathione Transferase (genetics), Glutathione transferase, Herbicides (toxicity), Humans, Interaction, Male, Middle Aged, Modification, Nervous system diseases, Occupational Exposure, Paraquat (toxicity), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (epidemiology), Parkinson Disease, Secondary (genetics), Parkinson disease, Pesticides, Questionnaires, Risk Factors.
MESH :
- chemical , genetics : Glutathione Transferase.
- chemically induced : Disease Susceptibility, Parkinson Disease, Secondary.
- epidemiology : Disease Susceptibility, Parkinson Disease, Secondary.
- genetics : Parkinson Disease, Secondary.
- chemical , toxicity : Herbicides, Paraquat.
- Age Factors, Aged, Aged, 80 and over, Case-Control Studies, Cohort Studies, Diagnosis, Computer-Assisted, Female, Gene Deletion, Genetic Association Studies, Genotype, Humans, Male, Middle Aged, Occupational Exposure, Questionnaires, Risk Factors.

Abstract

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 glutathioneS-transferaseMl (GSTM1)orT1 (GSTT1). Eighty-seven 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-person examination. Paraquat use and covariates were determined by interview. We genotyped subjects for homozygous deletions of GSTM1 (GSTM1^*0) and GSTT1 (GSTT1^*0) and tested interaction between paraquat use and genotype using logistic regression. Two hundred and twenty-three (52%) subjects had GSTM1^*0, 95 (22%) had GSTT1^*0, and 73 (17%; all men) used paraquat. After adjustment for potential confounders, there was no interaction with GSTM1. In contrast, GSTT1 genotype significantly modified the association between paraquat and PD. In men with functional GSTT1, the odds ratio (OR) for association of PD with paraquat use was 1.5 (95% confidence interval [CI]: 0.6-3.6); in men with GSTT1^*0, the OR was 11.1 (95% CI: 3.0-44.6; P interaction: 0.027). Although replication is needed, our results suggest that PD risk from paraquat exposure might be particularly high in individuals lacking GSTT1. GSTT1^*0 is common and could potentially identify a large subpopulation at high risk of PD from oxidative stressors such as paraquat.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572192

Affiliations:

Allemagne, Argentine, Canada, États-Unis
Californie, Caroline du Nord, Hawaï, Maryland, Ontario
Toronto
Université de Toronto

Le document en format XML

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<wicri:noRegion>Lübeck</wicri:noRegion>
<wicri:noRegion>University of Lübeck</wicri:noRegion>
<wicri:noRegion>Lübeck</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Chade, Anabel R" sort="Chade, Anabel R" uniqKey="Chade A" first="Anabel R." last="Chade">Anabel R. Chade</name>
<affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Institute of Cognitive Neurology, Institute of Neuroscience, Favaloro University</s1>
<s2>Buenos Aires</s2>
<s3>ARG</s3>
<sZ>11 aut.</sZ>
</inist:fA14>
<country>Argentine</country>
<wicri:noRegion>Buenos Aires</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Comyns, Kathleen" sort="Comyns, Kathleen" uniqKey="Comyns K" first="Kathleen" last="Comyns">Kathleen Comyns</name>
<affiliation wicri:level="2"><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
<country>États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Richards, Marie B" sort="Richards, Marie B" uniqKey="Richards M" first="Marie B." last="Richards">Marie B. Richards</name>
<affiliation wicri:level="2"><inist:fA14 i1="08"><s1>Westat Inc.</s1>
<s2>Durham, North Carolina</s2>
<s3>USA</s3>
<sZ>13 aut.</sZ>
</inist:fA14>
<country>États-Unis</country>
<placeName><region type="state">Caroline du Nord</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sandler, Dale P" sort="Sandler, Dale P" uniqKey="Sandler D" first="Dale P." last="Sandler">Dale P. Sandler</name>
<affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park</s1>
<s2>North Carolina</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
<country>États-Unis</country>
<placeName><region type="state">Caroline du Nord</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Blair, Aaron" sort="Blair, Aaron" uniqKey="Blair A" first="Aaron" last="Blair">Aaron Blair</name>
<affiliation wicri:level="2"><inist:fA14 i1="09"><s1>Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS</s1>
<s2>Bethesda, Maryland</s2>
<s3>USA</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
<country>États-Unis</country>
<placeName><region type="state">Maryland</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="William Langston, J" sort="William Langston, J" uniqKey="William Langston J" first="J." last="William Langston">J. William Langston</name>
<affiliation wicri:level="2"><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
<country>États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tanner, Caroline M" sort="Tanner, Caroline M" uniqKey="Tanner C" first="Caroline M." last="Tanner">Caroline M. Tanner</name>
<affiliation wicri:level="2"><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
<country>États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Case-Control Studies</term>
<term>Cohort Studies</term>
<term>Diagnosis, Computer-Assisted</term>
<term>Disease Susceptibility (chemically induced)</term>
<term>Disease Susceptibility (epidemiology)</term>
<term>Environment</term>
<term>Female</term>
<term>Gene Deletion</term>
<term>Genetic Association Studies</term>
<term>Genotype</term>
<term>Glutathione Transferase (genetics)</term>
<term>Glutathione transferase</term>
<term>Herbicides (toxicity)</term>
<term>Humans</term>
<term>Interaction</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Modification</term>
<term>Nervous system diseases</term>
<term>Occupational Exposure</term>
<term>Paraquat (toxicity)</term>
<term>Parkinson Disease, Secondary (chemically induced)</term>
<term>Parkinson Disease, Secondary (epidemiology)</term>
<term>Parkinson Disease, Secondary (genetics)</term>
<term>Parkinson disease</term>
<term>Pesticides</term>
<term>Questionnaires</term>
<term>Risk Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutathione Transferase</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Disease Susceptibility</term>
<term>Parkinson Disease, Secondary</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Disease Susceptibility</term>
<term>Parkinson Disease, Secondary</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease, Secondary</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Herbicides</term>
<term>Paraquat</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Age Factors</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Case-Control Studies</term>
<term>Cohort Studies</term>
<term>Diagnosis, Computer-Assisted</term>
<term>Female</term>
<term>Gene Deletion</term>
<term>Genetic Association Studies</term>
<term>Genotype</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Occupational Exposure</term>
<term>Questionnaires</term>
<term>Risk Factors</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term>
<term>Pathologie du   système nerveux</term>
<term>Modification</term>
<term>Glutathione transferase</term>
<term>Pesticide</term>
<term>Environnement</term>
<term>Interaction</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Pesticide</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">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 glutathioneS-transferaseMl (GSTM1)orT1 (GSTT1). Eighty-seven 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-person examination. Paraquat use and covariates were determined by interview. We genotyped subjects for homozygous deletions of GSTM1 (GSTM1<sup>*</sup>
0) and GSTT1 (GSTT1<sup>*</sup>
0) and tested interaction between paraquat use and genotype using logistic regression. Two hundred and twenty-three (52%) subjects had GSTM1<sup>*</sup>
0, 95 (22%) had GSTT1<sup>*</sup>
0, and 73 (17%; all men) used paraquat. After adjustment for potential confounders, there was no interaction with GSTM1. In contrast, GSTT1 genotype significantly modified the association between paraquat and PD. In men with functional GSTT1, the odds ratio (OR) for association of PD with paraquat use was 1.5 (95% confidence interval [CI]: 0.6-3.6); in men with GSTT1<sup>*</sup>
0, the OR was 11.1 (95% CI: 3.0-44.6; P interaction: 0.027). Although replication is needed, our results suggest that PD risk from paraquat exposure might be particularly high in individuals lacking GSTT1. GSTT1<sup>*</sup>
0 is common and could potentially identify a large subpopulation at high risk of PD from oxidative stressors such as paraquat.</div>
</front>
</TEI>
<affiliations><list><country><li>Allemagne</li>
<li>Argentine</li>
<li>Canada</li>
<li>États-Unis</li>
</country>
<region><li>Californie</li>
<li>Caroline du Nord</li>
<li>Hawaï</li>
<li>Maryland</li>
<li>Ontario</li>
</region>
<settlement><li>Toronto</li>
</settlement>
<orgName><li>Université de Toronto</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Californie"><name sortKey="Goldman, Samuel M" sort="Goldman, Samuel M" uniqKey="Goldman S" first="Samuel M." last="Goldman">Samuel M. Goldman</name>
</region>
<name sortKey="Bhudhikanok, Grace S" sort="Bhudhikanok, Grace S" uniqKey="Bhudhikanok G" first="Grace S." last="Bhudhikanok">Grace S. Bhudhikanok</name>
<name sortKey="Blair, Aaron" sort="Blair, Aaron" uniqKey="Blair A" first="Aaron" last="Blair">Aaron Blair</name>
<name sortKey="Comyns, Kathleen" sort="Comyns, Kathleen" uniqKey="Comyns K" first="Kathleen" last="Comyns">Kathleen Comyns</name>
<name sortKey="Hoppin, Jane A" sort="Hoppin, Jane A" uniqKey="Hoppin J" first="Jane A." last="Hoppin">Jane A. Hoppin</name>
<name sortKey="Kamel, Freya" sort="Kamel, Freya" uniqKey="Kamel F" first="Freya" last="Kamel">Freya Kamel</name>
<name sortKey="Korell, Monica" sort="Korell, Monica" uniqKey="Korell M" first="Monica" last="Korell">Monica Korell</name>
<name sortKey="Meng, Cheryl" sort="Meng, Cheryl" uniqKey="Meng C" first="Cheryl" last="Meng">Cheryl Meng</name>
<name sortKey="Richards, Marie B" sort="Richards, Marie B" uniqKey="Richards M" first="Marie B." last="Richards">Marie B. Richards</name>
<name sortKey="Sandler, Dale P" sort="Sandler, Dale P" uniqKey="Sandler D" first="Dale P." last="Sandler">Dale P. Sandler</name>
<name sortKey="Tanner, Caroline M" sort="Tanner, Caroline M" uniqKey="Tanner C" first="Caroline M." last="Tanner">Caroline M. Tanner</name>
<name sortKey="Umbach, David M" sort="Umbach, David M" uniqKey="Umbach D" first="David M." last="Umbach">David M. Umbach</name>
<name sortKey="Webster Ross, G" sort="Webster Ross, G" uniqKey="Webster Ross G" first="G." last="Webster Ross">G. Webster Ross</name>
<name sortKey="William Langston, J" sort="William Langston, J" uniqKey="William Langston J" first="J." last="William Langston">J. William Langston</name>
</country>
<country name="Canada"><region name="Ontario"><name sortKey="Marras, Connie" sort="Marras, Connie" uniqKey="Marras C" first="Connie" last="Marras">Connie Marras</name>
</region>
</country>
<country name="Allemagne"><noRegion><name sortKey="Kasten, Meike" sort="Kasten, Meike" uniqKey="Kasten M" first="Meike" last="Kasten">Meike Kasten</name>
</noRegion>
</country>
<country name="Argentine"><noRegion><name sortKey="Chade, Anabel R" sort="Chade, Anabel R" uniqKey="Chade A" first="Anabel R." last="Chade">Anabel R. Chade</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

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Movement Disorders (revue)

Genetic Modification of the Association of Paraquat and Parkinson's Disease

Genetic Modification of the Association of Paraquat and Parkinson's Disease

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	Movement Disorders (revue)
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