Low selenium status affects arsenic metabolites in an arsenic exposed population with skin lesions.

ABSTRACT

BACKGROUND: The antagonistic effects between selenium (Se) and arsenic (As) suggest that low selenium status plays important roles in arsenism development. However, no study has been reported for humans suffering from chronic arsenic exposure with low selenium status. METHODS: Sixty-three subjects were divided into 2 experimental groups by skin lesions (including hyperkeratosis, depigmentation, and hyperpigmentation). Total urine and serum concentrations of arsenic and selenium were determined by ICP-MS with collision/reaction cell. Arsenic species were analysed by ICP-MS coupled with HPLC. RESULTS: The mean concentration of As in the drinking waters was 41.5 microg/l. The selenium dietary intake for the studied population was 31.7 microg Se/d, and which for the cases and controls were 25.9 and 36.3 microg Se/d, respectively. Compared with the controls, the skin lesions cases had lower selenium concentrations in serum and urine (41.4 vs 49.6 microg/l and 71.0 vs 78.8 microg/l, respectively), higher inorganic arsenic (iAs) in serum (5.2 vs 3.4 microg/l, P<0.01), higher percentages of iAs in serum and urine (20.2) vs 16.9% and 18.3 vs 14.5%, respectively, P<0.01) but lower percentages of monomethylarsonate (MMA) in serum (15.5 vs 18.8%, P<0.01) ans dimethylarsinate acid (DMA) in urine (65.1 vs 69.8%, P<0.01). Subjects with lower selenium concentrations in serum (<50 microg/l) had a stronger tendency to the risk of skin lesions than individual having higher selenium concentrations [odd ratio (OR), 7.3; 95% confidence interval (95% CI), 1.5-35.7; P=0.014]. This OR estimation was confirmed in those subjects having higher ratios of As/Se in urine and serum, with OR as high as 10.3 and 3.8 respectively. CONCLUSIONS: Lower serum selenium status (<50 microg/l) is significantly correlated to the arsenic-associated skin lesions in the arsenic exposed population. The accumulation of iAs and its inhibition to be biotransformed to DMA occurred in human due to chronic exposure of low selenium status.