论文部分内容阅读
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。
Objective To investigate the mechanism of cadmium toxicity in renal injury. Methods Wistar rats were injected intraperitoneally with a mixture of CdCl2 and mercaptoethanol to prepare animal model of cadmium poisoning kidney injury. The rats were exposed to selenium and the selenium was administered to selenium in renal cells Trace element distribution and lipid peroxidation level changes. Results After exposure to cadmium, the content of selenium and antioxidant enzyme in mitochondria and cytosol of rat kidney cells decreased significantly, while the contents of oxygen free radicals and malondialdehyde (MDA) increased. The distribution of some essential trace elements in the cells abnormal. Conclusion Selenium can restore GSH-Px activity of cadmium reduced to normal level, enhanced lipid peroxidation is inhibited, and the damaged renal function and ultrastructure are significantly improved .