【摘要】 目的　探讨 2 -乙氧基乙醇对肝脏的损伤机制。方法　对小鼠进行 2 -乙氧基乙醇腹腔注射亚慢性染毒并观察小鼠肝脏生化代谢的改变。结果　肝脏一氧化氮含量、一氧化氮合成酶活性自第 1周开始比对照组明显增加 (P<0 .0 5 ) ,二者实验组第 2 ,3,4周均比第 1周实验组显著增加 (P<0 .0 1) ;超氧化物歧化酶活性自第 3周开始比对照组和第 1周实验组显著增强 (P<0 .0 1) ;脂质过氧化产物丙二醛含量自第 2周开始比对照组和第 1周实验组显著增加 (P<0 .0 1) ,上述指标呈良好时间 -效应关系。染毒组血清谷丙转氨酶活性自第 1周起比对照组显著升高 (P<0 .0 5 ) ,第 4周回落。结论2 -乙氧基乙醇能引起肝脏一氧化氮自由基增加并诱发脂质过氧化反应对肝脏发生毒性作用。更多还原

【Abstract】 Objective To examine the mechanism of damage induced by 2 ethoxyethanol to hepatocytes.Methods 2 ethoxyethanol was administered via abdominal to mice at an interval of 2 days for 4 weeks. Then the changes of indices of lipid peroxidation were observed.Results NO’S contents and NOS’s were significantly larger than the control group from the first week ( P <0 05), and the NO’s contents and NOS’s activity of the exposure group in the second, third and fourth week were significantly larger than those of the exposuer group in the first week ( P <0 01). From the third week, the SOD’s activity was significantly higher than the control group and the first week’s exposure group ( P <0 01). The contents of MDA were significantly greater than the control group and the first week’s exposure group from the second week ( P <0 01). The serum level of GPT was significantly increased from the first week ( P <0 05), but declined in the fourth week.Conclusion The study demonstrated that 2 ethoxyethanol can increase the liver level of NO free radicals and the lipid peroxidation may play an important role in 2 ethoxyethanol’s liver toxicity.更多还原