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目的探讨氧自由基在急性镉中毒性肾损伤中的作用。方法给大鼠腹腔注射ＣｄＣｌ２（１５μｍｏｌ／ｋｇ）与巯基乙醇（３００μｍｏｌ／ｋｇ）混合液制备急性镉中毒性肾损伤模型，观察染镉后不同时间肾细胞线粒体、胞浆中一系列脂质过氧化指标的变化，同时测定肾皮质镉含量，检测肾功能和肾脏超微结构的改变。结果染镉后２小时肾皮质镉含量已达峰值；超微结构出现改变；氧自由基生成及丙二醛（ＭＤＡ）含量亦显著高于对照组（Ｐ＜０．０１），超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力下降。至染镉后１２小时，氧自由基产生及脂质过氧化反应达到高峰；肾功能损害亦十分明显；线粒体、溶酶体等细胞器严重受损。结论氧自由基大量生成及由此引起的脂质过氧化反应可能在镉对肾组织的损害中起重要作用。
Objective To investigate the role of oxygen free radicals in renal injury induced by acute cadmium poisoning. Methods Rat models of acute kidney injury induced by cadmium were prepared by intraperitoneal injection of a mixture of CdCl2 (15μmol / kg) and mercaptoethanol (300μmol / kg). The changes of mitochondria and cytosolic lipid peroxidation Index changes, while determination of renal cortex cadmium content, renal function and renal ultrastructure changes. Results The level of cadmium in renal cortex reached a peak at 2 hours after cadmium dyed, the ultrastructure was changed, the generation of oxygen free radicals and the content of malondialdehyde (MDA) were also significantly higher than those in the control group (P <0.01) Enzyme (SOD), glutathione peroxidase (GSH-Px) activity decreased. At 12 hours after cadmium exposure, the production of oxygen free radicals and lipid peroxidation peaked, and the renal dysfunction was also very obvious. Organelles, lysosomes and other organelles were severely damaged. Conclusion The massive generation of oxygen free radicals and the resulting lipid peroxidation may play an important role in the damage of kidney to cadmium.