三硝基甲苯中毒性白内障动物模型的建立及其发病机理的初步研究  

Cataract in Rat Induced by TNT and Machenism of its Formation

作　　者：黄莉莉[1] 贾维红[1] 杨涛[1] 张昌颖[1] 李风鸣[2] 吴惠群[2] 

机构地区：[1]北京医科大学生化教研室 [2]北京医科大学第三附属医院眼科教研室

出　　处：《生物化学杂志》1989年第4期375-381,共7页

摘　　要：反复多次给大鼠皮下注射20％三硝基甲苯(TNT)甘油:水混悬液,染毒15个月后21％动物发生白内障,其裂隙灯检查结果与人TNT性白内障基本相似,同时注射甘油:水溶剂的对照组大鼠无一例发生白内障。染毒10个月的大鼠,其晶状体LPO增高,GSH-P_X及GST活性降低,GR活性无变化,而GSH含量明显增加;注射TNT后肝脏LPO值、GSH含量、GSH-P_X、GR及GST活性均明显增高。本文结果提示,TNT中毒性白内障的形成可能系TNT及其代谢产物直接作用于晶状体,造成昌状体氧化损伤所致。TNT白内障大鼠模型的建立亦为深入探讨其发病机理及防治奠定了基础。Frequent injections of TNT over a period of 15 months caused cataract 21.4% of the rats. Slit lamp examination showed that the changes in lenses of rats with cataract were similar to those of TNT-cataract in man. In the rats receiving the injections of TNT for 10 months, lens LPO increased to 1.1-1 times of the control, activities of GSH-Px and GST decreasad evidently, but returned to normal levels shortly after stopping of TNT injections; no change was observerved in GR activity, and the glutathione content of lens was increased to about 109% of the normal. In liver, LPO, glutathione level, resaults imply that TNT-eataract formation may be induced by the action of TNT or its metabolites on lens through oxidative demages.

关 键 词：三硝基甲苯 白内障 谷胱甘肽 

分 类 号：R776.102[医药卫生—眼科]