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为探讨急性镉中毒后自由基产生和损伤的部位及机理，给予大鼠尾静脉注射氯化镉建立急性镉中毒模型，电镜观察自由基过氧化氢（Ｈ２Ｏ２） 的定位及细胞损伤，并测定抗氧化酶和氧化剂的变化。结果表明：Ｈ２Ｏ２ － ＣｅＣｌ３ 的阳性颗粒沉积在肝细胞膜上，最早出现在中毒后１ｈ，３ｈ 最严重，２４ｈ 消失；抗氧化酶活力受抑，以３ｈ 最严重（ｐ＜ ０－０１） ，６ｈ 后渐渐恢复；而ＧＳＨ 的含量在３ｈ 前均高于正常（ｐ ＜ ０－０５），以后逐步减少。提示自由基是急性镉中毒所致肝脏损伤的重要因素。
To investigate the site and mechanism of free radical generation and injury after acute cadmium poisoning, cadmium chloride was injected into the tail vein of rats to establish acute cadmium poisoning model. The localization and cell damage of free radical hydrogen peroxide (H2O2) were observed under electron microscope. Changes in oxidase and oxidant. The results showed that the positive particles of H2O2 - CeCl3 were deposited on the membrane of hepatocytes, the earliest appeared at 1h, 3h after poisoning and disappeared at 24h; the activity of antioxidant enzyme was inhibited at 3h (p <0-01) Gradually recovered; while the content of GSH in 3h before were higher than normal (p <0-05), and then gradually reduced. Prompted free radicals is an important factor in liver injury caused by acute cadmium poisoning.