氯化汞的肝细胞毒性与脂质过氧化

Mercury Toxicity and Lipid Peroxidation in Isolated Hepatocytes

本文研究了氯化汞对大鼠游离肝细胞的毒性及其与膜脂质过氧化和细胞内巯基含量的关系。结果显示,氯化汞具有明显的肝细胞毒性,呈现时间-效应和剂量-效应关系,其产生明显细胞毒性的最低剂量(5 μmol/L)低于其使细胞内巯基耗损的最低剂量,表明巯基的耗损并非其毒性的原因;应用抗氧化剂二苯基对苯二胺抑制氯化汞的脂质过氧化能力,并不能使肝细胞免于氯化汞的毒性作用,从而证实脂质过氧化亦非氯化汞毒性的原因,而仅为一种伴随现象。

Relationship between the hepatotoxicity and lipid peroxidation was studied in isolated rat hepatocytes. The results showed that mercuric chloride (HgCl2) exerts its toxici-ty on hepatocytes in a time- and dose-dependent fashion and the lowest concentration of Hg-Cl2 at which cytotoxicity becomes evident is 5 μmol/L. Reduced glutathione and protein thi-ols content also declined in the presence of the higher concentration of HgCl2, suggesting this decline to be a manifestation of the toxic response. The addition of the antioxidant N. N-diphenyl-p-phenylenediamine to the cell suspensions inhibited the HgCl2-induced lipid peroxidation, but did not cause any reduction in the HgQ2 toxicity in isolated hepatocytes. This finding indicates that lipid peroxidation is not directly responsible for the cell injury.