Ma X L, Baraona E, Lasker J M, Lieber C S
Section of Liver Disease and Nutrition, Bronx Veterans Affairs Medical Center, New York, NY 10468.
Biochem Pharmacol. 1991 Jul 15;42(3):585-91. doi: 10.1016/0006-2952(91)90321-u.
To study the effects of ethanol on the hepatotoxicity of N-nitrosodimethylamine (NDMA), 5 mg NDMA/kg body weight was injected intraperitoneally 3 times a week for 6 weeks into rats pair-fed liquid diets containing 36% of energy either as ethanol or as additional carbohydrates. Another group of rats was pair-fed with the same diets but injected with saline instead of NDMA. Co-administration of ethanol and NDMA produced much higher elevations of serum alanine and aspartate aminotransferase and glutamic dehydrogenase activities than the administration of either agent alone. The combined treatment also slightly increased focal necrosis, whereas other liver lesions (steatosis and fibrosis) and the functional impairment of mitochondrial respiration were not affected significantly. Microsomal low Km NDMA demethylation, as well as NDMA denitrosation, were inhibited markedly by incubation with an antibody against P450IIE1, suggesting the involvement of this alcohol-inducible P450 in both NDMA bioactivation reactions. The addition of ethanol inhibited P450-dependent demethylation and denitrosation of NDMA in liver microsomes, whereas both activities were enhanced markedly by chronic ethanol administration. At ethanol concentrations similar to those prevailing in the blood of alcohol-fed animals at the time of NDMA administration, hepatic microsomal demethylation and denitrosation remained significantly higher in ethanol-fed rats given NDMA than in controls. Our results suggest that bioactivation plays a critical role in the hepatotoxicity of NDMA and its aggravation by chronic alcohol consumption.
为研究乙醇对N-亚硝基二甲胺(NDMA)肝毒性的影响,将5mg NDMA/千克体重每周腹腔注射3次,持续6周,注射于成对喂养含36%能量的液体饮食的大鼠,该能量来源要么是乙醇,要么是额外的碳水化合物。另一组大鼠成对喂养相同饮食,但注射生理盐水而非NDMA。与单独给予任何一种药物相比,乙醇与NDMA共同给药导致血清丙氨酸和天冬氨酸转氨酶以及谷氨酸脱氢酶活性升高幅度大得多。联合治疗也轻微增加了局灶性坏死,而其他肝脏病变(脂肪变性和纤维化)以及线粒体呼吸功能损害未受到显著影响。微粒体低Km NDMA去甲基化以及NDMA脱亚硝化作用,通过与抗P450IIE1抗体孵育而被显著抑制,提示这种酒精诱导的P450参与了两种NDMA生物活化反应。乙醇的添加抑制了肝微粒体中P450依赖的NDMA去甲基化和脱亚硝化作用,而慢性给予乙醇则显著增强了这两种活性。在与给予NDMA时酒精喂养动物血液中相似的乙醇浓度下,给予NDMA的乙醇喂养大鼠的肝微粒体去甲基化和脱亚硝化作用仍显著高于对照组。我们的结果提示生物活化在NDMA的肝毒性及其因慢性酒精摄入而加重中起关键作用。