摘要
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 。
Objective To study the mechanism of cadmium induced renal oxidative damage. Methods Rats were exposed to CdCl 2(0.65 or 2.28 mg/kg) by subcutaneous injection once per day for 5 sucessive days.Superoxide dismutase(SOD)mRNA expression and SOD activity were determined at different time after exposure,at the same time cadmium concentration of renal cortex was analyzed and the kidney ultrastruture was examined. Results The mitochondria of renal proximal tubular cells in two exposed groups were damaged first,and their SOD mRNA expression levels were lower than that in control group 6 h after exposure.The scanning integral at spot print showed significant difference between the control group(70?928±7?698) and the high dose group(35 400±5 900),or the low dose group(35 919±7 361), P <0.01.In the low dose group,the expression of SOD mRNA almost recovered to the level of control group 72 h after exposure.The reduction in SOD activity appeared after morphological change and inhibition of mRNA transcription. Conclusion Inhibition of SOD gene expression may be one of the important factors to cause renal damage by cadmium.Low dose cadmium induced renal damage with the change mentioned above may be recovered.
出处
《中华劳动卫生职业病杂志》
CAS
CSCD
北大核心
2001年第2期91-94,共4页
Chinese Journal of Industrial Hygiene and Occupational Diseases
