title: Pesticide exposure on southwestern Taiwanese with MnSOD and NQO1 polymorphisms is associated with increased risk of Parkinson's disease.
abstract: BACKGROUND
  Hypothetic mechanism of the individual vulnerability to oxidative stress through metabolism of environmental xenobiotics and genotypic polymorphisms has been considered to promote the development of Parkinson's disease (PD). In this case-control study, we determined the role of manganese-containing superoxide dismutase (MnSOD) and NAD(P)H: quinone oxidoreductase 1 (NQO1) genes in PD risk in a population with high prevalence of pesticide exposure.
  
  
  METHODS
  From southwestern region of Taiwan, we enrolled 153 patients with idiopathic PD and 155 healthy control subjects matched for age, sex and origin. Detailed questionnaires of face-to-face interviews among these subjects were collected. PCR-based restriction fragment length polymorphism (RFLP) assays were used to determine the genotypes of MnSOD (-9 T>C) and NQO1 (609 C>T) genes.
  
  
  RESULTS
  Exposure to pesticides associated with PD was significant among patients with an increased odds ratio (OR) of 1.69 (95%CI, 1.07-2.65), and this association remained significant after adjustment for age, sex, and cigarette smoking (aOR=1.68, 95%CI, 1.03-2.76, P=0.023). Considering genetic factors, there were no significant differences in frequencies of both genotypes of MnSOD and NQO1 polymorphisms between PD patients and the control subjects (P>0.05). However, this difference in genotype distribution was significant among subjects who had been exposed to pesticide, with aOR of 2.49 (95%CI, 1.18-5.26, P=0.0072) for MnSOD C allele and aOR of 2.42 (95%CI, 1.16-4.76, P=0.0089) for NQO1 T allele, respectively. Moreover, among subjects exposed to pesticide, the combined MnSOD/NQO1 variant genotype was significantly associated with a 4.09-fold increased risk of PD (95%CI, 1.34-10.64, P=0.0052).
  
  
  CONCLUSIONS
  Susceptible variants of MnSOD and NQO1 genes may interact with occupational pesticide exposure to increase PD risk in southwestern Taiwanese.
authors.affiliation: Department of Neurology, Buddhist Dalin Tzu Chi General Hospital, Chia-Yi, and National Taiwan University Hospital, Taipei, Taiwan.
authors.forename: Chin-Shih
authors.initials: CS
authors.lastname: Fong
authors.forename: Ruey-Meei
authors.initials: RM
authors.lastname: Wu
authors.forename: Jia-Ching
authors.initials: JC
authors.lastname: Shieh
authors.forename: Ya-Ting
authors.initials: YT
authors.lastname: Chao
authors.forename: Yi-Ping
authors.initials: YP
authors.lastname: Fu
authors.forename: Chiz-Liang
authors.initials: CL
authors.lastname: Kuao
authors.forename: Chun-Wen
authors.initials: CW
authors.lastname: Cheng
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D004781:Environmental Exposure; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000235:genetics*; D010300:Parkinson Disease / Q000209:etiology*; D010575:Pesticides / Q000633:toxicity*; D011110:Polymorphism, Genetic; D017382:Reactive Oxygen Species; D012306:Risk; D013482:Superoxide Dismutase / Q000235:genetics*
chemical_list: D010575:Pesticides; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D016660:NAD(P)H Dehydrogenase (Quinone); C447479:NQO1 protein, human