Abstract
BackgroundChronic arsenic exposure is associated with an increased risk of skin, bladder and lung cancers. Generation of oxidative stress may contribute to arsenic carcinogenesis.MethodsTo investigate the association between arsenic exposure and oxidative stress, urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was evaluated in a cohort of 97 women recruited from an arsenic-endemic region of Bangladesh in 2003. Arsenic exposure was measured in urine, toenails, and drinking water. Drinking water and urine samples were collected on three consecutive days. Susceptibility to oxidative stress was evaluated by genotyping relevant polymorphisms in glutathione-s transferase mu (GSTM1), human 8-oxoguanine glycosylase (hOGG1) and apurinic/apyrimidinic endonuclease (APE1) genes using the Taqman method. Data were analyzed using random effects Tobit regression to account for repeated measures and 8-OHdG values below the detection limit.ResultsA consistent negative effect for APE1 was observed across water, toenail and urinary arsenic models. APE1 148 glu/glu + asp/glu genotype was associated with a decrease in logged 8-OHdG of 0.40 (95%CI -0.73, -0.07) compared to APE1 148 asp/asp. An association between total urinary arsenic and 8-OHdG was observed among women with the GSTM1 null genotype but not in women with GSTM1 positive. Among women with GSTM1 null, a comparison of the second, third, and fourth quartiles of total urinary arsenic to the first quartile resulted in a 0.84 increase (95% CI 0.27, 1.42), a 0.98 increase (95% CI 033, 1.66) and a 0.85 increase (95% CI 0.27, 1.44) in logged 8-OHdG, respectively. No effects between 8-OHdG and toenail arsenic or drinking water arsenic were observed.ConclusionThese results suggest the APE1 variant genotype decreases repair of 8-OHdG and that arsenic exposure is associated with oxidative stress in women who lack a functional GSTM1 detoxification enzyme.
Highlights
Arsenic, a naturally occurring element, is a common environmental contaminant
We investigated whether chronic arsenic exposure was associated with oxidative stress by evaluating the association between total urinary arsenic (TUA), toenail arsenic and drinking water arsenic and urinary Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) concentration among a cohort of Bangladeshi women who did not exhibit any cutaneous signs of arsenic toxicity and were exposed to a wide range of arsenic concentrations in drinking water
Subjects were eligible for this study if they were long-term residents of Pabna, obtained their drinking water from tube wells, and received primary health care from the Pabna Community Clinic, an affiliate of Dhaka Community Hospital (DCH)
Summary
A naturally occurring element, is a common environmental contaminant. Elevated concentrations can occur in drinking water, the primary route of exposure, through natural and anthropogenic process. The most affected region is Bangladesh, where an estimated 29 to 40 million people are at risk of ingesting arsenic-contaminated drinking water [1]. One hypothesized mechanism involves the induction of oxidative stress through the generation of reactive oxygen species (ROS) [3]. Mice that have been administered the arsenic metabolite dimethylarsinic acid (DMA V) orally and topically have developed skin tumors and shown increased levels of 8-hydroxyguanine in the epidermis [7]. Chronic arsenic exposure is associated with an increased risk of skin, bladder and lung cancers. Generation of oxidative stress may contribute to arsenic carcinogenesis
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