氯化汞、氯化甲基汞对大鼠肾近曲小管细胞损伤机理的研究

TOXICITY OF MERCURIC CHLORIDE AND METHYLMERCURIC CHLORIDE IN ISOLATED RAT RENAL PROXIMAL TUBULES

研究了HgCl_2和CH_3HgCl对大鼠游离肾近曲小管细胞的毒性作用及其机理.结果显示,HgCl_2和CH_3HgCl均对肾细胞有明显毒性,表现为细胞内乳酸脱氢酶(LDH)和溶酶体β-葡糖苷酸酶(β-GD)漏出增加,还原型谷胱甘肽(GSH)和蛋白巯基(PSH)含量降低,同时GSH和PSH含量的降低与LDH及β-GD漏出之间呈良好的相关关系.未观察到CH_3HgCl明显诱发肾细胞脂质过氧化作用,HgCl_2仅在50μmol/L以上才出现轻度脂质过氧化效应.

Toxicity and cellular mechanisms of mercuric chloride and methylmercuric chloride were studied in isolated rat renal proximal tubules. It was found that both mercuric chloride and methylmercuric chloride can result in the increase of release of intracellular enzymes, lactate dehydrogenase and β-glucuronidase, into incubation medium and depletion of cellular reduced glutathione and protein thiols in a time- and dose-dependent manner. In addition,the depletion of cellular thiols, both reduced glutatione and protein thiols, were closely related to the loss of lactate dehydrogenase and β-glucuronidase. No obvious lipid pe-roxidation was observed in response to mercuric chloride and methylmercuric chloride. These results indicate that the depletion of thiols may be responsible for cell injury and lipid peroxidation is not.