砷
亚砷酸盐
谷胱甘肽
蛋氨酸
甲基化
化学
亚砷酸钠
口服
无机砷
排泄
地下水砷污染
砷中毒
体内
砷毒性
生物化学
药理学
生物
氨基酸
酶
生物技术
有机化学
基因
作者
Yaping Jin,Fenghong Zhao,Yuan Zhong,Xiaoyun Yu,Di Sun,Yingjun Liao,Xiuqiang Lv,Gexin Li,Guifan Sun
摘要
We hypothesized that chronic exposure to arsenic would deplete the reduced glutathione (GSH) and methionine in vivo, thereby impair the methylation capacity of inorganic arsenic (iAs) ingested. Our experiment was designed to explore the effects of exogenous GSH and methionine on arsenic methylation in mice exposed to arsenite via drinking water. Levels of iAs, monomethylarsenic acid (MMAs), and dimethylarsenic acid (DMAs) in the liver and blood were determined by the method of hydride generation coupled with atomic absorption spectrophotometry. Compared with mice exposed to arsenite alone, administration of GSH or methionine increased the secondary methylation index in the liver and primary methylation index in the blood, which resulted in the consequent increase of DMAs percent and decrease of iAs percent in the blood. Moreover, administration of GSH resulted in the increase of DMAs percent in the liver and total arsenic in the blood. Increase of total arsenic in the blood was mainly due to the increase of DMAs. Findings from the present study suggested that administration of GSH or methionine might potentiate the methylation capacity of arsenic in both liver and extrahepatic tissues, which may facilitate the excretion of arsenic and decrease arsenic related toxicities in the body.
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