Evidence for induction of oxidative stress caused by chronic exposure of Chinese residents to arsenic contained in drinking water.

Evidence for induction of oxidative stress caused by chronic exposure of Chinese residents to arsenic contained in drinking water.
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DOI:
10.1289/ehp.02110331
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发表时间:
2002-04
影响因子:
10.4
通讯作者:
Shimojo N
Shimojo N
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Pi J;Yamauchi H;Kumagai Y;Sun G;Yoshida T;Aikawa H;Hopenhayn-Rich C;Shimojo N

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实验动物或培养的细胞暴露于砷诱导氧化应激,但迄今为止,还没有关于人类这种现象的研究报告。本研究在中国内蒙古五原进行了一项横断面研究,探讨饮用水慢性砷暴露与人体氧化应激之间的关系。33名饮用高浓度无机砷(平均值为0.41 mg/L)管井水18年的居民为高暴露组,10名居住在附近但饮用低浓度无机砷(平均值为0.02 mg/L)的居民为低暴露对照组。本研究结果表明,虽然血液中的超氧化物歧化酶(SOD)的活性没有显着差异,高暴露组与低暴露组相比,血清脂质过氧化物(LPO)的平均水平显着较高。血清LPO浓度升高与血中无机砷及其甲基化代谢物水平相关。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平均血NPSH水平比低砷暴露组低57.6%。血中NPSH水平与血中无机砷及其甲基化代谢产物的浓度和单甲基砷与无机砷的比值呈负相关。这些结果提供的证据表明,慢性暴露于砷从饮用水中的人类的氧化应激的诱导结果,如减少NPSH和LPO的增加。对砷诱导的氧化应激的可能机制进行了讨论。
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.
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