title: GST polymorphisms, interaction with smoking and pesticide use, and risk for Parkinson's disease in a Japanese population.
abstract: Patients with idiopathic Parkinson's disease (PD) appear to have reduced capacity for detoxification of certain environmental compounds. The glutathione S-transferases (GSTs) are candidate genes for PD because they are involved in the metabolism of pesticides and cigarette smoke. We investigated the relationship of the seven GST polymorphisms (GSTM1 deletion, GSTT1 deletion, GSTP1 rs1695, GSTO1 rs4925, GSTO1 rs11191972, GSTO2 rs156697 and GSTO2 rs2297235) and PD risk with special reference to the interaction with pesticide use or cigarette smoking among 238 patients with PD cases and 370 controls in a Japanese population. None of the GST polymorphisms were associated with PD. GSTO1 rs4925 and GSTO2 rs2297235 were found to be in strong linkage disequilibrium (D' = 0.98). Cigarette smoking was significantly associated with decreased risk of PD. However, no interaction of smoking with any of the GST polymorphisms was observed. Self-reported pesticide use was not associated with increased risk of PD. There was no evidence of interaction between self-reported pesticide use and either GST polymorphism. Our results suggest that the tested GST polymorphisms did not play an important role in PD susceptibility in our Japanese population. Our study does not give evidence of interaction between the GST polymorphisms and smoking may although this study provided sufficient statistical power to detect modest interaction. As for interaction between GSTP polymorphisms and pesticide use, the power of this study to detect an interactive effect was low due to a small number of pesticide users. Future studies involving larger control and case populations and better pesticide exposure histories will undoubtedly lead to a more thorough understanding of the role of the GST polymorphisms in PD development.
authors.affiliation: Department of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan. chikako@phealth.med.kyushu-u.ac.jp
authors.forename: C
authors.initials: C
authors.lastname: Kiyohara
authors.forename: Y
authors.initials: Y
authors.lastname: Miyake
authors.forename: M
authors.initials: M
authors.lastname: Koyanagi
authors.forename: T
authors.initials: T
authors.lastname: Fujimoto
authors.forename: S
authors.initials: S
authors.lastname: Shirasawa
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
authors.forename: W
authors.initials: W
authors.lastname: Fukushima
authors.forename: S
authors.initials: S
authors.lastname: Sasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Tsuboi
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Oeda
authors.forename: T
authors.initials: T
authors.lastname: Miki
authors.forename: N
authors.initials: N
authors.lastname: Kawamura
authors.forename: N
authors.initials: N
authors.lastname: Sakae
authors.forename: H
authors.initials: H
authors.lastname: Fukuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Hirota
authors.forename: M
authors.initials: M
authors.lastname: Nagai
mesh_terms: D000368:Aged; D004781:Environmental Exposure / Q000009:adverse effects; D005260:Female; D055106:Genome-Wide Association Study; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics*; D006801:Humans; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010300:Parkinson Disease / Q000209:etiology / Q000235:genetics / Q000523:psychology; D010575:Pesticides / Q000009:adverse effects*; D011110:Polymorphism, Genetic / Q000235:genetics*; D044382:Population Groups; D012189:Retrospective Studies; D012307:Risk Factors; D012907:Smoking
chemical_list: D010575:Pesticides; D005982:Glutathione Transferase