Casini A F, Ferrali M, Pompella A, Maellaro E, Comporti M
Am J Pathol. 1986 Jun;123(3):520-31.
The mechanisms of bromobenzene toxicity in extrahepatic tissues of mice were studied. Kidney, lung, heart and brain were examined. As observed in this as well as in a previous report for the liver, bromobenzene intoxication caused a progressive decrease in the glutathione content of all the tissues examined. Cellular damage (as assessed by both biochemical determinations and histologic observations) appeared after 6 hours in the case of the kidney and the heart and after 15 hours in the case of the lung. Lipid peroxidation (as assessed by the tissue content of malonic dialdehyde, a parameter correlating with both the diene conjugation absorption and the amount of carbonyl functions in cellular phospholipids) was found to occur at the same times at which cellular damage was observed or even before. As in the case of bromobenzene-induced liver injury, when the individual values for cell damage obtained at 15-20 hours were plotted against the corresponding glutathione contents, a severe cellular damage was generally observed when the glutathione levels reached a threshold value (3.0-0.5 nmol/mg protein). Such a glutathione threshold was also observed for the onset of lipid peroxidation. Glutathione depletion and lipid peroxidation are therefore general phenomena occurring not only in the liver but in all the tissues as a consequence of bromobenzene poisoning. The possibility that lipid peroxidation is the cause of bromobenzene-induced damage to liver and extrahepatic tissues is discussed.
研究了溴苯对小鼠肝外组织的毒性机制。对肾脏、肺、心脏和大脑进行了检查。正如本研究以及之前关于肝脏的报告中所观察到的，溴苯中毒导致所有检查组织中的谷胱甘肽含量逐渐下降。肾脏和心脏在6小时后出现细胞损伤（通过生化测定和组织学观察评估），肺在15小时后出现细胞损伤。脂质过氧化（通过丙二醛的组织含量评估，丙二醛是与二烯共轭吸收以及细胞磷脂中羰基功能数量相关的参数）在观察到细胞损伤的同时甚至之前就已发生。与溴苯诱导的肝损伤情况一样，当将15 - 20小时获得的细胞损伤个体值与相应的谷胱甘肽含量作图时，当谷胱甘肽水平达到阈值（3.0 - 0.5 nmol/mg蛋白质）时，通常会观察到严重的细胞损伤。脂质过氧化的发生也观察到了这样一个谷胱甘肽阈值。因此，谷胱甘肽耗竭和脂质过氧化是溴苯中毒不仅在肝脏而且在所有组织中都会出现的普遍现象。本文讨论了脂质过氧化是否是溴苯诱导肝脏和肝外组织损伤的原因。
