1,2 - 二溴乙烷对离体肝细胞的影响：功能改变及脂质过氧化诱导

Effects of 1,2-dibromoethane on isolated hepatocytes: functional alterations and induction of lipid peroxidation.

van Iersel A A, van Holsteijn I, Blaauboer B J

Department of Veterinary Pharmacology, Pharmacy and Toxicology, University of Utrecht, The Netherlands.

Xenobiotica. 1988 Jun;18(6):675-83. doi: 10.3109/00498258809041706.

Abstract

Isolated rat hepatocytes were exposed to the fumigant 1,2-dibromoethane (DBE) and cytotoxicity was evaluated by studying parameters of cellular function and lipid peroxidation. 2. DBE caused plasma membrane damage, as determined by leakage of lactate dehydrogenase, and was more severe in shaken suspensions than stationary suspensions, suggesting that cells were more fragile after DBE exposure. 3. DBE decreased hepatocyte glycogen content and stimulated albumin synthesis in hepatocyte suspensions. 4. Lipid peroxidation resulted from DBE exposure and was greater in cells isolated from phenobarbital-pretreated rats. Shaking the suspensions enhanced lipid peroxidation. Ethane production did not parallel formation of thiobarbituric acid reactants, suggesting that these parameters of lipid peroxidation reflect different mechanisms of molecular interaction of DBE.

摘要

将分离的大鼠肝细胞暴露于熏蒸剂1,2 - 二溴乙烷（DBE），并通过研究细胞功能参数和脂质过氧化来评估细胞毒性。2. 如通过乳酸脱氢酶泄漏所测定的，DBE导致质膜损伤，并且在振荡悬浮液中比静止悬浮液中更严重，这表明DBE暴露后细胞更脆弱。3. DBE降低了肝细胞糖原含量，并刺激了肝细胞悬浮液中白蛋白的合成。4. DBE暴露导致脂质过氧化，并且在从苯巴比妥预处理的大鼠分离的细胞中脂质过氧化更严重。振荡悬浮液增强了脂质过氧化。乙烷的产生与硫代巴比妥酸反应物的形成不平行，这表明脂质过氧化的这些参数反映了DBE分子相互作用的不同机制。