镉性肾损伤时肾皮质细胞中微量元素与脂质过氧化改变  

Changes in trace elements and lipid peroxidation of renal cortical cells in nephrotoxic damage of Cadmium

作　　者：龙曼海[1,2,3,4,5] 赵金垣[1,2,3,4,5] 王世俊 刘爱萍[1,2,3,4,5] 邵涵如 刘亚宁[1,2,3,4,5] 

机构地区：[1]贵阳医学院预防医学系 [2]北京医科大学第三医院职业病研究中心 [3]包头医学院预防医学教研室 [4]中国科学院高能物理研究所 [5]空军总医院检验科发光室

出　　处：《中华劳动卫生职业病杂志》1998年第1期26-29,共4页Chinese Journal of Industrial Hygiene and Occupational Diseases

基　　金：国家自然科学基金;美国中华医学基金

摘　　要：目的探讨镉中毒性肾损伤的机制。方法用ＣｄＣｌ２与巯基乙醇的混合液给予Ｗｉｓｔａｒ大鼠一次腹腔注射染毒，制备镉中毒性肾损伤的动物模型，并投用微量元素硒，观察大鼠染毒及给硒后的肾细胞内的微量元素分布及脂质过氧化水平的变化。结果染镉后，大鼠肾细胞线粒体、胞液内硒含量、抗氧化酶活力明显降低，而氧自由基与丙二醛（ＭＤＡ）水平升高；某些必需微量元素在细胞内的分布出现异常。结论加硒可使被镉降低的谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力恢复至正常水平，增强的脂质过氧化反应受抑制，受损的肾功能及超微结构得到明显改善。To study the mechanism of nephrotoxic damage of cadmium,an experimental renal damage model was made by a single ip injection of CdCl^2+ME in Wistar rat.At the same time selenium was given.The results showed that after Cd was given,Se levels and the activities of antioxidase in mitochondria and cytosol of renal cortical cells were lower than those of control group,and the levels of oxygen free radicals and MDA were higher than those of control.The distribution of some essential trace elements in renal cortical cells was abnormal.When Se was given,the activity of GSHPx reduced by Cd could be restored to normal.The elevated levels of lipid peroxidation induced by Cd were reduced.Se could also improve the abnormal renal function and the ultrastructure caused by Cd.

关 键 词：镉中毒 肾损伤 微量元素 脂质过氧化 肾皮质细胞 

分 类 号：R135.1[医药卫生—劳动卫生] R692.02[医药卫生—公共卫生与预防医学]