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目的研究脂质过氧化和自由基在急性镉中毒性肝脏损伤中的作用及金属硫蛋白（ＭＴ）的保护作用。方法测定镉染毒后不同时间大鼠肝脏的ＭＴ和脂质过氧化产物丙二醛（ＭＤＡ）的含量及抗氧化酶的活力，观察肝细胞超微结构的损伤，进行自由基（Ｈ２Ｏ２）的定位。结果大鼠急性染镉后ＭＤＡ高于对照组（Ｐ＜０．０５）；抗氧化酶活力在３小时显著受抑（Ｐ＜０．０５），６小时明显恢复；ＭＴ在３小时即有增加，６小时达正常组的６．７倍；肝细胞膜上Ｈ２Ｏ２的阳性沉积物３小时最严重，２４小时已消失，但此时细胞损伤最严重，４８小时肝细胞再生、修复。结论镉可引起肝脏脂质过氧化及自由基的大量产生，抑制抗氧化酶的活力，造成细胞的严重损伤。ＭＴ对肝脏抗氧化酶活力的恢复、脂质过氧化的减轻、自由基的清除及损伤的肝细胞的保护可能有重要作用。
Objective To investigate the role of lipid peroxidation and free radicals in acute cadmium poisoning liver injury and the protective effect of metallothionein (MT). Methods The contents of MT and lipid peroxidation product malondialdehyde (MDA) and antioxidant enzyme activity in rat liver were measured at different time points after exposure to cadmium. The ultrastructural damage of hepatocytes was observed and the content of free radical (H2O2) Positioning. Results The level of MDA in acute exposure to cadmium in rats was significantly higher than that in control group (P <0.05). The antioxidant enzyme activity was significantly inhibited at 3 hours (P <0.05), significantly restored at 6 hours, and MT increased at 3 hours , 6 hours up to 6.7 times the normal group; liver cell membrane H2O2 positive sediment 3 hours the most serious, 24 hours have disappeared, but this time the most serious cell damage, 48 hours of liver regeneration, repair. Conclusion Cadmium can cause liver lipid peroxidation and a large number of free radicals, inhibit the activity of antioxidant enzymes, resulting in serious cell damage. MT may play an important role in the restoration of liver antioxidant enzyme activity, the reduction of lipid peroxidation, the clearance of free radicals and the protection of damaged hepatocytes.