氧化应激致慢性水砷暴露小鼠肝损伤作用  

Effect of oxidative stress in hepatic injury in oral drinking arsenic exposed mice

作　　者：蒋玲[1] 李玲[1] 吴君[2] 欧兵[2] 张韵[2] 李诚秀[1] 程明亮[2] 杨勤[3] 

机构地区：[1]贵阳医学院药理教研室,贵阳550004 [2]贵阳医学院附属医院感染科 [3]贵阳医学院病理生理教研室

出　　处：《中国公共卫生》2008年第5期593-595,共3页Chinese Journal of Public Health

基　　金：国家自然科学基金项目(30471592);科技部国际科技合作与交流专项经费项目〔2005DFA30640(A类)〕

摘　　要：目的比较不同价态的砷对小鼠脐组织中谷胱甘肽过氧化物酶(GSH-Px)和胎盘型谷胱甘肽-S-转移酶(GST-Pi)表达的影响,探讨氧化应激在慢性砷暴露致肝损伤中的作用。方法60只雄性昆明种小鼠,体重(20±2)g,随机分为对照组、亚砷酸钠组和砷酸钠组。染毒10个月后处死小鼠,检测血清肝功能;测定肝组织总砷含量;做病理检查;Trizol-酚-氯仿一步法提取小鼠肝组织总RNA,紫外分光光度法测定总RNA浓度及纯度。逆转录PCR(RT-PCR)技术测定小鼠肝组织中GSH-Px和GST-Pi mRNA的表达,以18S基因作为质控。结果亚砷酸钠组在肝组织中的砷蓄积量〔(3992±250)ng/g组织〕高于砷酸钠组〔(2603±357)ng/g组织〕(P<0.05);砷暴露组的肝组织病理检查显示有明显组织损伤;与对照组比较,亚砷酸钠组的血清丙氨酸转氨酶(ALT)〔(61.46±13.85)U/L〕、天冬氨酸转氨酶(AST)〔(510.86±59.01)U/L〕、球蛋白(Glb)〔(26.94±3.73)g/C)〕L值均显著升高,肝组织中GST-Pi mRNA的表达(163.3±11.6)降低,P<0.05。结论砷致小鼠肝损伤与砷在肝组织中的蓄积有关。氧化应激可能是慢性饮水砷中毒致小鼠肝损伤的机制之一。Objective To compare the expression and its significance of glutathione peroxidase （GSH- Px） and glutathione - S - transferase （ GST - Pi） in hepatic tissue in oral drinking arsenic exposed mice. Methods 60 mice were divided into control group, sodium arsenite group and sodium arsenate group at random. The mice were sacrificed after 10 month for the liver function, total arsenic detection and pathologic examination. Extract the total RNA of hepatic tissue and detect its density and purity, detect the expression of GSH - Px and GST - Pi mRNA with real time fluorescence quantitative PCR and the result was controlled with 18s. Results Arsenic accumulation in sodium arsenite group [ （3 992 ± 250）ng/g tissue] was higher than that of sodium arsenite group [2 603 ±357ng/gtissue, P 〈 0.05]. Pathologic examinations showed that there were notable liver cell necrosis and regeneration. Serum ALT [61.46 ± 13.85], U/L. AST [ （ 510.86±59.0） IU/L]. G1 b [ （ 26.94 ±3.73）g/L] in sedium arsenite group was higher than that of the normal group, while the expression of GST- Pi mRNA （163.3 ± 11.6） was lower（ P 〈05）. Conclusion There were relationship between hepatic injury and arsenic accumulation. Oxidative stress may be the one of significant effects in the process of hepatic injury caused by oral drinking arsenic exposure in mice.

关 键 词：饮水砷暴露 肝损伤 谷胱甘肽过氧化物酶 谷胱甘肽-S-转移酶 逆转录PCR 

分 类 号：R599[医药卫生—内科学]