Strubelt O, Obermeier F, Siegers C P, Vöpel M
Toxicology. 1978 Jul;10(3):261-70. doi: 10.1016/0300-483x(78)90076-8.
Male rats provided with a 5 or 15% (v/v) ethanol solution as the sole source of fluid consumed ethanol at a rate of 11.4 or 24.9% of total calories (4.2 or 8.3 g/kg daily). After ethanol consumption lasting 1, 2 and 3 weeks the hepatotoxicity of CCl4 (0.1 ml/kg i.p.) was elevated by determination of serum activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase ( GPT), sorbitol dehydrogenase (SDH) and histological investigations. Carbon tetrachloride (CCl4)-induced liver damage was significantly greater in rats provided with ethanol than in the tap-water consuming controls. This potentiation of CCl4 hepatotoxicicty was fully developed already after a 1-week exposition to ethanol and was greater in the 15% than in the 5% ethanol group. Ethanol alone did not influence serum enzyme activities but increased microsomal aniline hydroxylation. There was, however, no clear-cut parallelism between potentiation of CCl4 hepatotoxicity and activation of aniline hydroxylation.
给雄性大鼠提供5%或15%（v/v）的乙醇溶液作为唯一的液体来源，它们消耗乙醇的速率分别为总热量的11.4%或24.9%（每日4.2或8.3克/千克）。在持续摄入乙醇1周、2周和3周后，通过测定血清谷氨酸草酰乙酸转氨酶（GOT）、谷氨酸丙酮酸转氨酶（GPT）、山梨醇脱氢酶（SDH）的活性以及进行组织学研究，发现四氯化碳（0.1毫升/千克，腹腔注射）的肝毒性增强。与饮用自来水的对照组相比，摄入乙醇的大鼠中四氯化碳（CCl4）诱导的肝损伤明显更严重。在接触乙醇仅1周后，四氯化碳肝毒性的这种增强作用就已充分显现，且在15%乙醇组中比5%乙醇组更明显。单独的乙醇并不影响血清酶活性，但会增加微粒体苯胺羟化作用。然而，四氯化碳肝毒性的增强与苯胺羟化作用的激活之间并没有明显的平行关系。
