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目的研究腹腔注射硫酸铍对小鼠肝脏的毒性作用,探讨硫酸铍致肝脏毒性的可能机制。方法将30只6周龄昆明种雄性小鼠随机分为3组,分别以1和2 mg/kg硫酸铍灭菌生理盐水溶液腹腔注射染毒,对照组用灭菌生理盐水溶液腹腔注射。隔日1次,连续染毒2周。检测血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)水平;测定小鼠肝脏脏器系数、肝脏线粒体肿胀程度、肝脏线粒体中丙二醛(MDA)含量、线粒体谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)活性;观察肝脏病理组织学变化。结果与对照组比较,硫酸铍染毒组小鼠肝脏脏器系数、血清中AST和ALT水平随剂量增加而增高,差异有统计学意义(P<0.05);染毒组小鼠肝脏线粒体肿胀明显、肝线粒体MDA含量显著增高(P<0.05),GSH-Px活性、SOD活性随染毒剂量的增加而降低(P<0.05);病理组织学检查可见肝细胞广泛变性、坏死。结论硫酸铍致小鼠肝毒性作用明显,线粒体脂质过氧化可能是硫酸铍致肝毒性机制之一。
Objective To study the toxic effects of intraperitoneal injection of beryllium sulphate on the liver of mice and to explore the possible mechanism of liver toxicity induced by beryllium sulfate. Methods Thirty male Kunming mice of 6 weeks old were randomly divided into 3 groups. The mice were inoculated intraperitoneally with 1 and 2 mg / kg beryllium sulfate sterile saline, respectively. The control group was injected intraperitoneally with sterile saline solution. 1 every other day for 2 consecutive weeks. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured. The liver organ coefficient, swelling degree of liver mitochondria, malondialdehyde (MDA) content in liver mitochondria and mitochondrial glutathione peroxidase GSH-Px) and superoxide dismutase (SOD) activity. The histopathological changes of liver were observed. Results Compared with the control group, the liver organ coefficient and serum AST and ALT levels increased with the dose increasing in beryllium sulphate-treated mice (P <0.05), and the mitochondria swelling in the liver of mice exposed to beryllium sulfate (P <0.05). The activity of GSH-Px and the activity of SOD decreased with the increase of the dose (P <0.05). The histopathological examination showed extensive degeneration and necrosis of hepatocytes. Conclusion Buplenyl sulfate induced obvious hepatotoxicity in mice. Mitochondrial lipid peroxidation may be one of the hepatotoxic mechanisms induced by beryllium sulfate.