title: Elevated risk of hypertension induced by arsenic exposure in Taiwanese rural residents: possible effects of manganese superoxide dismutase (MnSOD) and 8-oxoguanine DNA glycosylase (OGG1) genes.
abstract: Heavy metals, including arsenic and lead, may lead to cellular oxidative damage that is linked to hypertension. Manganese superoxide dismutase (MnSOD) is a scavenger of reactive oxygen species, and 8-oxoguanine DNA glycosylase (OGG1) is the major glycosylase that repairs DNA lesions. Interestingly, whether there is an elevated risk of hypertension with arsenic or lead exposure in individuals with genetic variations in MnSOD or OGG1 has not yet been investigated. Questionnaires were administered to 240 Taiwanese rural residents. Blood pressure and biochemical indicators were assessed in each subject. Urinary levels of arsenic and lead were measured with atomic absorption spectrometry; and MnSOD and OGG1 genotypes were identified via polymerase chain reaction. There was a dose-response relationship between urinary arsenic levels and risk of hypertension (P = 0.021, test for trend). However, there was no association between urinary lead levels and hypertension risk. Individuals with high urinary arsenic levels and the MnSOD Val-Ala/Ala-Ala genotypes had a greater risk of hypertension than those with low urinary arsenic levels and the MnSOD Val-Val genotype (odds ratio [OR] = 4.2, 95% confidence interval [CI] = 1.7-10.3). Subjects with a high urinary arsenic level and the OGG1 Cys-Cys genotype also had a greater risk of hypertension than those with a low urinary arsenic level and the OGG1 Ser-Ser/Ser-Cys genotypes (OR = 3.4, 95% CI = 1.1-10.7). Thus, both MnSOD and OGG1 genotypes may be prone to an increased risk of hypertension associated with arsenic exposure.
authors.affiliation: Department of Family and Community Medicine, Chung Shan Medical University Hospital, No. 110 Chien-Kuo N Rd, Sec. 1, Taichung 40242, Taiwan.
authors.forename: Shiuan-Chih
authors.initials: SC
authors.lastname: Chen
authors.forename: Chun-Chieh
authors.initials: CC
authors.lastname: Chen
authors.forename: Chung-Yih
authors.initials: CY
authors.lastname: Kuo
authors.forename: Chun-Huang
authors.initials: CH
authors.lastname: Huang
authors.forename: Chin-Hsiu
authors.initials: CH
authors.lastname: Lin
authors.forename: Zi-Yun
authors.initials: ZY
authors.lastname: Lu
authors.forename: Yi-Yu
authors.initials: YY
authors.lastname: Chen
authors.forename: Hong-Shen
authors.initials: HS
authors.lastname: Lee
authors.forename: Ruey-Hong
authors.initials: RH
authors.lastname: Wong
mesh_terms: D000328:Adult; D000368:Aged; D001151:Arsenic / Q000633:toxicity* / Q000652:urine; D003430:Cross-Sectional Studies; D045647:DNA Glycosylases / Q000235:genetics*; D004305:Dose-Response Relationship, Drug; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D005838:Genotype; D006147:Guanine / Q000031:analogs & derivatives / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000453:epidemiology / Q000235:genetics* / Q000652:urine; D007854:Lead / Q000633:toxicity / Q000652:urine; D008297:Male; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects / Q000706:statistics & numerical data; D018384:Oxidative Stress / Q000235:genetics; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012424:Rural Population / Q000706:statistics & numerical data*; D013482:Superoxide Dismutase / Q000235:genetics*; D013624:Taiwan / Q000453:epidemiology
chemical_list: D007854:Lead; D006147:Guanine; C064582:8-oxyguanine; D013482:Superoxide Dismutase; D045647:DNA Glycosylases; D001151:Arsenic