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目的 探讨镉对肾氧化损伤的作用机制。方法 Wistar大鼠皮下注射CdCl2 水溶液 ,每次剂量分别为 0 .6 5和 2 .2 8mg/kg ,连续染毒 5d ,观察染毒后不同时间肾超氧化物歧化酶 (SOD)活力及其mRNA表达水平变化 ,同时检测肾皮质镉含量、肾脏超微结构的改变。结果 染毒组肾近曲小管上皮细胞线粒体最早受到损伤 ,同时观察到SODmRNA表达明显低于对照组 ,斑点印迹扫描积分高剂量、低剂量组分别为 35 40 0± 5 90 0、35 919± 736 1,与对照组 (70 92 8± 76 98)比较 ,差异均有显著性 (P<0 .0 1)。SODmRNA的表达在停止染毒后有恢复的趋势 ,低剂量组染毒后 72h已基本恢复到对照组水平。SOD活力下降在形态改变和mRNA转录受抑制之后才出现。结论 SOD基因表达受抑制可能是镉性肾损伤的重要原因之一 ,低剂量镉引起的上述肾损伤有可能恢复
Objective To investigate the mechanism of cadmium on renal oxidative damage. Methods Wistar rats were subcutaneously injected CdCl2 aqueous solution at a dose of 0.56 and 2.2.8 mg / kg respectively for 5 days. The activities of renal superoxide dismutase (SOD) and its mRNA Expression level changes, while detecting renal cortex cadmium content, renal ultrastructure changes. Results The mitochondria of renal proximal tubule epithelial cells were the first to be injured and the expression of SODmRNA was significantly lower than that of the control group. The high-dose and low-dose spots of dot blot scoring were 35 40 ± 5 90 0, 35 919 ± 736 1, compared with the control group (70 92 8 ± 76 98), the difference was significant (P <0.01). The expression of SODmRNA tended to recover after stopping the exposure. The low dose group recovered to the control level 72h after exposure. Decreased SOD activity occurs only after morphological changes and suppression of mRNA transcription. Conclusions Inhibition of SOD gene expression may be one of the important causes of cadmium-induced renal injury. The renal damage caused by low-dose cadmium may be restored