Danni O, Aragno M, Ugazio G
Dipartimento di Medicina e Oncologia Seprimentale, Sezione di Patologia Ambientale, Torino, Italy.
Res Commun Chem Pathol Pharmacol. 1988 Sep;61(3):377-90.
Investigation of the hepatotoxicity of a mixture of two halogen compounds--carbon tetrachloride (CT) and 1,2-dibromoethane (DBE) used in association, especially in agriculture--is reported. Their simultaneous administration in the rat potentiates the necrosis provoked by exposure to CT alone. This damage can be totally prevented by prior treatment with vitamin E, which raises the liver antioxidant level. Determination of the TBA-reacting substances released from the liver homogenates of animals treated with one or both substances also corroborates the importance of lipid peroxidation in the pathogenesis of this potentiation. Furthermore, no significant difference between poisoning by CT and CT + DBE is noted when liver GSH values are measured under the same experimental conditions. This finding rules out the possibility that potentiation is only the simply sum of the damage caused by the two compounds (lipid peroxidation due to a radical initiator for CT, depletion of GSH for DBE). It is thus something more than a mere combination of two mechanisms of action and further investigation is required to unravel its more complex pathogenesis.
据报道，对两种卤素化合物——四氯化碳（CT）和1,2 - 二溴乙烷（DBE）的混合物（特别是在农业中联合使用时）的肝毒性进行了研究。它们同时给予大鼠会增强单独接触CT所引发的坏死。这种损伤可以通过预先用维生素E治疗来完全预防，维生素E可提高肝脏抗氧化水平。对用一种或两种物质处理的动物肝脏匀浆中释放的TBA反应性物质的测定也证实了脂质过氧化在这种增强作用发病机制中的重要性。此外，在相同实验条件下测量肝脏谷胱甘肽（GSH）值时，未发现CT中毒和CT + DBE中毒之间有显著差异。这一发现排除了增强作用仅仅是两种化合物所造成损伤的简单相加（CT为自由基引发剂导致脂质过氧化，DBE导致GSH耗竭）的可能性。因此，它不仅仅是两种作用机制的简单组合，需要进一步研究以阐明其更复杂的发病机制。
