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大鼠吸入浓度为6.08mg/L的氯丁二烯4小时后,于2、12和24小时处死动物。染毒后2小时血清山梨醇脱氢酶活性即明显升高,继而丙氨酸转氨酶活性升高,前者增高的幅度大于后者。肝匀浆还原型谷胧甘肤含量明显下降,然后升高;脂质过氧化产物丙二醛形成增多,肝线粒体膜脂流动性下降,与线粒体酶结合的1一苯氨基一蔡一8一磺酸(ANS)荧光增强。表明氯丁二烯所致急性肝损害可能与氧化应激机理有关。
Four hours after the rats inhaled chloroprene at a concentration of 6.08 mg / L, animals were sacrificed at 2, 12 and 24 hours. 2 hours after exposure to serum sorbitol dehydrogenase activity was significantly increased, followed by alanine aminotransferase activity increased, the former increased more than the latter. Liver homogenate reduced glutathione content significantly decreased, and then increased; malondialdehyde formation of lipid peroxidation products increased, the mitochondrial membrane lipid fluidity decreased, combined with the mitochondrial enzyme 1-aniline a Caiyi 8 Sulfonic acid (ANS) fluorescence enhancement. The results suggest that acute liver injury induced by chloroprene may be related to the mechanism of oxidative stress.