中文摘要：

目的探讨外源性谷胱甘肽（glutathione,GSH）对饮水砷暴露小鼠体内不同组织器官砷形态分布的影响。方法将实验小鼠随机分为对照组、单纯染砷组及低、中和高剂量GSH干预组。小鼠经饮水染砷4周,并于最后一周,在染砷同时腹腔注射不同剂量GSH。末次注射后24 h处死小鼠,取血、肝和脑组织。分别检测无机砷（iAs）、一甲基胂（MMA）和二甲基胂（DMA）的含量。结果GSH干预组小鼠的肝和血中iAs和MMA含量及血和脑中总砷含量（TAs）与单纯染砷组比较显著下降。GSH干预组小鼠的肝和血一甲基化率（PMR）和二甲基化率（SMR）明显升高。其中,高剂量GSH干预组小鼠的肝PMR和SMR及血SMR与单纯染砷组比较差异显著。结论外源性GSH可以促进肝中iAs的甲基化,加速砷化物从机体的排泄,从而可减少血中砷化物的含量,进而降低脑中砷化物的蓄积。

英文摘要：

Objective To explore the effect of exogenous glutathione（GSH）on the distribution and the morphous of arsenic in various organs or tissues of mice exposed to arsenite through drinking water.Methods Mice were randomly divided into five groups,which were control group,arsenic exposure group,low dose GSH group,medium dose GSH group,and high dose GSH group,eight mice in each group.Mice in the experimental groups were exposed to sodium arsenite through drinking water contaminated with 50 mg/L arsenic for four consecutive weeks.At the fourth week,simultaneously with the arsenic exposure,200 mg/kg,400 mg/kg and 800 mg/kg GSH were intraperitoneally injected to the mice in group 3,4,5 respectively.Twenty-four hours after the cessation of GSH administration,mice were anaesthetized and rapidly killed,taking the samples of blood,liver and immediately for the detection of inorganic arsenic（iAs）,monomethyl arsine（MMA）and dimethyl arsine（DMA）with HG-AAS method.Results It was showed that the contents of iAs and MMA in liver and blood,as well as the total contents of arsenic（TAs）in blood and brain of GSH treated mice were all significantly lower than those of As exposed mice.Additionally,the primary methylation ratio（PMR）and the secondary methylation ratio（SMR）both in liver and blood were higher than those of As exposed mice;the differences of PMR and SMR in liver,and SMR in blood between high dose GSH treated mice and As-exposed mice were quite significant.Conclusions The results suggested that the exogenous GSH might promote the methylation of inorganic arsenic in liver,increase the excretion of arsenide from living body,thereby decrease the content of arsenide in blood and its deposition in brain.