【摘要】 目的　探讨利福平增加异烟肼肝毒性的机制。方法　分别测定异烟肼组、利福平组和联合用药组小鼠的血清谷丙转氨酶（ＧＰＴ）、肝指数、肝匀浆丙二醛（ＭＤＡ）含量、肝微粒体Ｐ４５０和线粒体Ｃａ~２＋ＡＴＰ活性，及肝病理检查，结果与对照组或实验组之间进行比较。结果　异烟肼和利福平联合用药组的ＭＤＡ、ＧＰＴ明显增高，线粒体Ｃａ~２＋ ＡＴＰ酶活性明显降低（Ｐ＜０．０５），且肝细胞坏死较为明显。结论　异烟肼和利福平联合用药后肝毒性增加与膜脂质过氧化、线粒体Ｃａ~２＋　ＡＴＰ酶受损及利福平诱导肝药酶有关。更多还原

【Abstract】 Objective To study the mechanism of hepatic toxic injury induced by combining isoniazid with rifampicin in mice. Methods The level of serum glutamic-pyruvic transaminase(GPT), liver index, content of Inalondialdehyde (MDA ) of liver homogenate, activity of hepatic microsome enzyme and mitochondrial membrane Ca~2+ ATP enzyme, and degree of liver cell injury were investigated in mice. Results Combining isoniazid with rifampicin could markedly increase the level of GPT, and content of MDA of liver homogenate and decrease the activity of mitochondrial membrane Ca~2+ ATP enzyme, and the degree of liver injury. Conclusions The increase of hepatic toxic injury induced by combining isoniazid with rifampicin in mice is related to membrane lipid peroxidation the injury of mitochondrial membrane Ca~2+ ATP enzyme, and increase of artivity of hepatic microsome enzyme.更多还原