Srinivasan S, Recknagel R O
J Lipid Res. 1971 Nov;12(6):766-7.
Liver microsomal lipid peroxidation has been observed in fatal human CCl(4) poisoning, in rats with fatty livers induced by CCl(4) or by yellow phosphorus, and in mice poisoned with 1,1,2,2-tetrachloroethane. These observations suggest the possibility that other instances of toxic liver injury may involve lipid peroxidation. Cases of acute, fatal, toxic liver injury (e.g., from halothane anesthesia) are not likely to occur at or near laboratories equipped to determine whether any lipid peroxidation might have taken place. The data presented indicate that rat livers may be stored frozen for at least 7 days with no demonstrable diminution in CCl(4)-induced conjugated diene absorption of liver microsomal lipids.
在人类四氯化碳中毒致死病例、四氯化碳或黄磷诱导的脂肪肝大鼠以及1,1,2,2 - 四氯乙烷中毒的小鼠中，均观察到肝微粒体脂质过氧化现象。这些观察结果提示，其他毒性肝损伤情况可能也涉及脂质过氧化。急性、致命性毒性肝损伤病例（如氟烷麻醉所致）不太可能在配备了可确定是否发生脂质过氧化的实验室或其附近发生。所呈现的数据表明，大鼠肝脏冷冻保存至少7天，四氯化碳诱导的肝微粒体脂质共轭二烯吸收无明显减少。
