摘要
本文对P4,NaAsO_2,CCl_4亚慢性肝损伤大鼠肝细胞线粒体,微粒体LDH同工酶进行聚丙烯酰胺凝胶电泳,光密度扫描定量,对其标志酶组化染色,微机图象定量分析,结果表明,三组动物肝小叶线粒体标志酶SDH活性均有下降,其中以CCl_4组SDH下降较迟.NaAsO_2组染毒第8wk可见线粒体LDH_5升高,染毒12wk LDH_(2,3)下降,LDH_5升高与对照组比较无显著性差异,但仍高于P_4组,各组间微粒体LDH同工酶和其标志酶G-6-P酶活性变化存在差异;P_4组微粒体LDH同工酶改变明显且较其他两组早。
Male Wistar rats were treated orally with white phosphorus (P4) 1.5 mg·kg-1, sodium arsenite (NaAsO2) 20 mg·kg-1 and carbon tetrachloride (CC14) 500 mg·kg-1, 3 times a week up to 12 wk, LDH isoenzymes in the liver, hepatocyte mitochondria and microsomes were separated by polyacrylamide gel electrophoresis and measured by soft scanning densitometer and the liver SDH and G-6-Pase were measured by the morphometry in histocytochemistry. The SDH in the liver lobule, used as mitochondrion marker enzyme, was decreased in the animals exposed to CC14, P4 and NaAsO2; the change of SDH in the rats exposed to CC14 was later than that of the others. In the rats exposed to NaAsO2, the LDH5 in mitochondria was elevated at 8 wk, LDH2 and LDH3 were decreased at 12 wk, G-6-Pase, used as a microsome marker enzyme, was increased in the central and middle zones of the liverlobule but decreased in the peripheral zone, and the LDH5 in microsomes was increased after 10 wk. In the rats exposed to CC14, G-6-Pase remained unchanged in the liver lobule; the LDH5 in microsomes was increased at 12 wk. In the rats exposed to P4, G-6-Pase was decreased in all the three zones and the total area of the liver lobule at 10 wk and increased in the middle and peripheral zones and the liver lobule at 12 wk; the LDH5 in microsomes was increased remarkably after 8 wk, and the change of LDH isoenzymes in microsomes in rats of the P4 group was taken place obviously and earlier than that in the other groups.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1992年第4期292-296,共5页
Chinese Journal of Pharmacology and Toxicology
基金
国家"七五"攻关课题
关键词
磷
砷
线粒体
乳酸脱氢酶
同功酶
phosphorus arsenic carbon tetrachloride liver mitochondria microsomes lactate dehydrogenase isoenzymes histocytoche mistry