三硝基甲苯在鼠肝线粒体中的还原活化及其对线粒体Ca^(2+)转运的影响  

Reductive activation of trinitrotoluene by rat liver mitochondria and its effect on ^(45)Ca transport

作　　者：庄志雄[1] 刘世杰[1] 江泉观[1] 

机构地区：[1]北京医科大学劳动卫生教研室

出　　处：《中国药理学与毒理学杂志》1990年第3期208-212,共5页Chinese Journal of Pharmacology and Toxicology

基　　金：国家"七五"攻关课题

摘　　要：在无氧条件下,以560μmol/L TNT与1mmol/L NADPH和大鼠肝线粒体(2 mg蛋白/ml)在室温下温育,用ESR波谱直接观察到TNT还原活化后形成的硝基阴离子自由基信号,信号的出现取决于温育体系中的所有三种成分。若温育体系中通入氧气,则信号消失。在有氧条件下,不同浓度TNT(35～560μmol/L)与NADPH及鼠肝线粒体在37℃温育,可致线粒体氧耗明显增加,伴有超氧阴离子自由基的形成和NADPH的氧化,线粒体对^(45)Ca的摄取能力也有明显的下降,这些改变均呈明显的浓度效应关系。当560μmol/L TNT加入到^(45)Ca预负荷的线粒体中,线粒体中的^(45)Ca释放明显增加,提示线粒体对Ca^(2+)的隔离功能受损。研究中还发现,在温育体系中加入超氧化物歧化酶和/或过氧化氢酶,可减少TNT引起的线粒体氧耗增加及NADPH氧化。Anaerobic incubation of 560μmol/L trinitrotoluene(TNT),an explosive applied widely in the munitions and mining industries,with 1 mmol/L NADPH and 2 mg rat liver mitochondria protein/ml produced an electron spin resonance(ESR)spectrum of nitro anion free radical.The radical formation depended on all three components in the incubation system.In the presence of oxygen,the similar incubation manifested no observable ESR signal.Aerobically,TNT-stimulated oxygen consumption,superoxide(O2-)formation,NADPH oxidation and inhibited45Ca uptake by mitochondria were shown in dose-dependent manner.Addition of TNT into the 45Ca preloading mitochondria resulted in the increased 45Ca release from them,suggesting the disrupted Ca2+ compartment function of mitochondria.It was also shown that SOD and/or CAT reduced TNT-stimulated oxygen consumption and NADPH oxidation by mitochondria.

关 键 词：三硝基甲苯 线粒体 还原活化 CA^2+ 

分 类 号：R992[医药卫生—毒理学]