Pi Jingbo, Yamauchi Hiroshi, Kumagai Yoshito, Sun Guifan, Yoshida Takahiko, Aikawa Hiroyuki, Hopenhayn-Rich Claudia, Shimojo Nobuhiro
Graduate School Doctoral Program in Medical Sciences, University of Tsukuba, Ibaraki, Japan.
Environ Health Perspect. 2002 Apr;110(4):331-6. doi: 10.1289/ehp.02110331.
Exposure of experimental animals or cultured cells to arsenic induces oxidative stress, but, to date, no examination of this phenomenon in humans has been reported. In this study we conducted a cross-sectional study in Wuyuan, Inner Mongolia, China, to explore the relationship between chronic arsenic exposure from drinking water and oxidative stress in humans. Thirty-three inhabitants who had been drinking tube-well water with high concentrations of inorganic arsenic (mean value = 0.41 mg/L) for about 18 years constituted the high-exposure group, and 10 residents who lived nearby but were exposed to much lower concentrations of arsenic in their drinking water (mean value = 0.02 mg/L) were selected as the low-exposure comparison group. Results of the present study indicated that although the activity for superoxide dismutase (SOD) in blood did not differ significantly between the two groups, the mean serum level of lipid peroxides (LPO) was significantly higher among the high-exposed compared with the low-exposed group. Elevated serum LPO concentrations were correlated with blood levels of inorganic arsenic and its methylated metabolites. In addition, they showed an inverse correlation with nonprotein sulfhydryl (NPSH) levels in whole blood. The subjects in the high-arsenic-exposure group had mean blood NPSH levels 57.6% lower than those in the low-exposure group. Blood NPSH levels were inversely correlated with the concentrations of inorganic arsenic and its methylated metabolites in blood and with the ratio of monomethylarsenic to inorganic arsenic. These results provide evidence that chronic exposure to arsenic from drinking water in humans results in induction of oxidative stress, as indicated by the reduction in NPSH and the increase in LPO. Some possible mechanisms for the arsenic-induced oxidative stress are discussed.
将实验动物或培养细胞暴露于砷会引发氧化应激，但迄今为止，尚未有关于人类这一现象的研究报道。在本研究中，我们在中国内蒙古五原县进行了一项横断面研究，以探讨饮用水中慢性砷暴露与人类氧化应激之间的关系。33名饮用高浓度无机砷（平均值 = 0.41毫克/升）管井水约18年的居民构成高暴露组，另外选取10名居住在附近但饮用水中砷暴露浓度低得多（平均值 = 0.02毫克/升）的居民作为低暴露对照组。本研究结果表明，虽然两组血液中超氧化物歧化酶（SOD）活性无显著差异，但高暴露组的脂质过氧化物（LPO）平均血清水平显著高于低暴露组。血清LPO浓度升高与血液中无机砷及其甲基化代谢产物水平相关。此外，它们与全血中非蛋白巯基（NPSH）水平呈负相关。高砷暴露组受试者的血液NPSH平均水平比低暴露组低57.6%。血液NPSH水平与血液中无机砷及其甲基化代谢产物浓度以及一甲基砷与无机砷的比例呈负相关。这些结果提供了证据，表明人类饮用水中慢性砷暴露会导致氧化应激的诱导，表现为NPSH减少和LPO增加。文中还讨论了砷诱导氧化应激的一些可能机制。
