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蒋玲, 李玲, 吴君, 欧兵, 张韵, 李诚秀, 程明亮, 杨勤. 氧化应激致慢性水砷暴露小鼠肝损伤作用[J]. 中国公共卫生, 2008, 24(5): 593-595. DOI: 10.11847/zgggws2008-24-05-40
引用本文: 蒋玲, 李玲, 吴君, 欧兵, 张韵, 李诚秀, 程明亮, 杨勤. 氧化应激致慢性水砷暴露小鼠肝损伤作用[J]. 中国公共卫生, 2008, 24(5): 593-595. DOI: 10.11847/zgggws2008-24-05-40
JIANG Ling, LI Ling, WU Jun, . Effect of oxidative stress in hepatic injury in oral drinking arsenic exposed mice[J]. Chinese Journal of Public Health, 2008, 24(5): 593-595. DOI: 10.11847/zgggws2008-24-05-40
Citation: JIANG Ling, LI Ling, WU Jun, . Effect of oxidative stress in hepatic injury in oral drinking arsenic exposed mice[J]. Chinese Journal of Public Health, 2008, 24(5): 593-595. DOI: 10.11847/zgggws2008-24-05-40

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

  • 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.

     

    Abstract: Objective Tocompare the expression and its significance of glutathione peroxidase(GSH-Px)and glu tathione-S-transferase(GST-Pi)in hepatictissue in oral drinking arsenicexposed mice.Methods 60 mice were divided intocontrol group,sodium arsenite group and sodium arsenate group atrandom.The mice were sacrificed after 10 month for the liverfunction,total arsenicdetection and patholog icexamination.Extractthe total RNA of hepatictissue and detectits density and purity,detectthe expression of GSH-Pxand GST-Pi mRNA with real time fluorescence quantitative PCR and the resultwas controlled with 18s.Results Arsenica ccumulation in sodium arsenite group(3 992±250)ng/g tissue was hig herthan thatof sodium arsenite group 2603±357ng/gtissue,P<0.05.Pathologicexaminations showed thatthere were notable livercell necrosis and regeneration.Serum AL T6.46±13.85,U/L.AST(510.86±59.0)I U/L.G1b(26.94±3.73)g/L in sedium arsenite group was higher than thatof the normal group,while the expression of GST-Pi mRNA(163.3±11.6)was lower(P<0.05).Conclusion There were relationship between hepaticinjury and arsenicaccumulation.Oxidative stress may be the one of sig nificanteffects in the process of hepaticinjury caused by oral drinking arsenicexposure in mice.

     

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