中文摘要：

采用不同浓度（50、100、200mg·kg-1）的联苯胺（Benzidine）和不同浓度（200、400、800mg·kg-1）的六氯苯（1,2,3,4,5,6-Hexachlorocyclohexane）,通过对大鼠进行体内染毒建立毒性作用动物模型,分析了大鼠肝脏线粒体抗氧化物酶及呼吸代谢和能量转换酶（SOD、GSH-Px、COX和Ca2＋-ATPase、Mg2＋-ATPase）活性的变化.结果表明,在低浓度联苯胺（50mg·kg-1）和六氯苯（200mg·kg-1或400mg·kg-1）作用下酶活性出现应激反应,而高浓度联苯胺（100、200mg·kg-1）和六氯苯（800mg·kg-1）则显示出明显的抑制作用.分析认为,联苯胺和六氯苯可能经体内代谢活化后,对线粒体DNA及其转录和翻译系统产生作用,导致线粒体代谢功能紊乱,这可能是联苯胺和六氯苯毒性作用对线粒体损伤的主要机制.

英文摘要：

We constructed an animal model to evaluate the toxic effects of benzidine（50,100,and 200mg·kg-1）and 1,2,3,4,5,6-hexachlorocyclohexane（200,400 and 800mg·kg-1）on enzyme activities of rat liver mitochonria.In this model,we analyzed the enzyme activity changes of oxide-resisting enzymes,breathing metabolization and energe-transfering enzymes（SOD,GSH-Px,COX,Ca2 ＋-ATPase and Mg2 ＋-ATPase）in mitochondria.Results showed that low doses of benzidine（50mg·kg-1）and 1,2,3,4,5,6-hexachlorocyclohexane（200mg·kg-1 or 400mg·kg-1）could induce the stress reaction and increase the enzyme activities,however,high doses of benzidine（100,200mg·kg-1）and 1,2,3,4,5,6-hexachlorocyclohexane（800mg·kg-1）significantly inhibited the enzyme activities.These results indicates that benzidine and 1,2,3,4,5,6-hexachlorocyclohexane may affect the transcription and translation of mitochondria DNA,and result in the damage of mitochonria.