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目的研究CCl4急性染毒小鼠肝细胞线粒体损伤的毒理机制。方法 ICR雄性小鼠,随机分为正常对照组,7.5、15、30和60 mg/kg CCl4组,腹腔注射16 h后测定小鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)活力和肝组织脂质过氧化产物丙二醛(MDA)水平,测定线粒体膜电位值、线粒体肿胀敏感度以及线粒体内游离钙的含量。结果与正常对照组相比,15、30和60 mg/kg CCl4组小鼠血清ALT、AST活力显著增高、肝组织MDA水平明显上升,各染毒组小鼠肝细胞线粒体膜电位值下降、线粒体肿胀的敏感性下降,同时检测到15、30和60 mg/kg CCl4组小鼠肝细胞线粒体内钙离子超载。随着染毒剂量的增大,CCl4对上述各指标的影响逐渐增加。结论在该试验条件下,CCl4毒理机制可能与线粒体内钙超载导致线粒体膜通透性转运孔(PTP)高通透性开放有关。
Aim To study the toxicological mechanism of mitochondrial damage induced by CCl4 in mice acute hepatotoxicity. Methods ICR male mice were randomly divided into normal control group, 7.5, 15, 30 and 60 mg / kg CCl4 groups. Serum alanine aminotransferase (ALT) and aspartate aminotransferase ) Activity and malondialdehyde (MDA) level of liver tissue lipid peroxidation products, mitochondrial membrane potential, mitochondrial swelling sensitivity and mitochondrial free calcium content. Results Compared with the normal control group, the ALT and AST activities of serum in CCl4, 15, 30 and 60 mg / kg groups were significantly increased, and the levels of MDA in liver tissue were significantly increased. The mitochondrial membrane potential The swelling sensitivity was also decreased. At the same time, mitochondrial Ca2 + overload was detected in liver cells of CCl4 at 15, 30 and 60 mg / kg. With the increase of dose, the influence of CCl4 on the above indexes gradually increased. Conclusion Under the experimental conditions, the toxic mechanism of CCl4 may be related to the overload of mitochondrial calcium resulting in the high permeability of the mitochondrial membrane permeability transition pore (PTP).