Botti B, Bini A, Calligaro A, Meletti E, Tomasi A, Vannini V
Toxicol Appl Pharmacol. 1986 May;83(3):494-505. doi: 10.1016/0041-008x(86)90232-2.
Diethylmaleate (DEM) potentiated the 1,2-dibromoethane (DBE)-induced hepatic morphological lesion in fasted male Wistar rats, as revealed by light and electron microscopy examination. The subcellular structures involved in such lesions were the mitochondria. The potentiating effect of DEM appeared to be due to enhancement of the depletion of hepatic mitochondrial glutathione (GSH) caused by DBE. DEM, however, failed to potentiate the DBE-induced release in the plasma of hepatic enzymes. The relationship between loss of mitochondrial GSH, mitochondrial injury, and the importance of the mitochondrial lesion in DBE-induced hepatotoxicity is discussed.
顺丁烯二酸二乙酯（DEM）增强了禁食雄性Wistar大鼠中1,2 - 二溴乙烷（DBE）诱导的肝脏形态学损伤，这通过光学和电子显微镜检查得以揭示。参与此类损伤的亚细胞结构是线粒体。DEM的增强作用似乎是由于增强了DBE引起的肝脏线粒体谷胱甘肽（GSH）耗竭。然而，DEM未能增强DBE诱导的肝脏酶在血浆中的释放。本文讨论了线粒体GSH丧失、线粒体损伤之间的关系以及线粒体损伤在DBE诱导的肝毒性中的重要性。
