ParkinsonCanadaV1, Main, Exploration, bibRecord, 001425

Genetic modification of the association of paraquat and Parkinson's disease

Identifieur interne : 001425 ( Main/Exploration ); précédent : 001424; suivant : 001426

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 ] ; 2012-11.

RBID : ISTEX:859AB96117C97280F4627C5B4A0835D85635B3D6

Descripteurs français

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

English descriptors

KwdEn :
- Environment, Glutathione transferase, Interaction, Modification, Nervous system diseases, Parkinson disease, Parkinson's disease, Pesticides, gene‐environment interaction, glutathione transferase, paraquat, pesticide.

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 glutathione S‐transferase M1 (GSTM1) or T1 (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. © 2012 Movement Disorder Society

Url:

DOI: 10.1002/mds.25216

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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<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 glutathione S‐transferase M1 (GSTM1) or T1 (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. © 2012 Movement Disorder Society</div>
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HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001425 | SxmlIndent | more

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{{Explor lien
   |wiki=    Wicri/Canada
   |area=    ParkinsonCanadaV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     ISTEX:859AB96117C97280F4627C5B4A0835D85635B3D6
   |texte=   Genetic modification of the association of paraquat and Parkinson's disease
}}

This area was generated with Dilib version V0.6.29.
Data generation: Thu May 4 22:20:19 2017. Site generation: Fri Dec 23 23:17:26 2022

La maladie de Parkinson au Canada (serveur d'exploration)

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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	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.