亚慢性镉中毒肝损伤的实验病理研究  

Pathological study of subchronic cadmium-induced hepatic injury.

作　　者：陶炼晖 王翔朴[1] 何坚[2] 唐外星 

机构地区：[1]湖南医科大学环境医学研究室 [2]湖南医科大学病理学教研室 [3]湖南医科大学电镜室

出　　处：《职业医学》1990年第2期67-70,126-127,共4页China Occupational Medicine

摘　　要：本文动态观察了亚慢性镉中毒大鼠肝组织中镉含量,组织学及超微结构改芰。特点:肝细胞内多种亚微结构受损;核内包涵体形成;狄氏间隙微绒毛消失。给镉早期线粒体肿胀、空泡变性,粗面内质网(RER)与糖原聚集成片及毛细胆管破坏等:随后糖原逐渐减少、消失,RER、线粒体扩张破坏,次级溶酶体增加和狄氏腔内胶原纤维增生。肝细胞坏死早期较明显。肝组织内镉含量显著增高,但未发现镉离子富集现象,提示镉在肝组织内以结合形式存在。Using a model of subchronic Cd-induced hepatic injury of male Wistar rats treated with CdCl_2(0.592mg Cd^(2+)/kg body wt. ip., 5 times a week up to 9 weeks), histological and ultrastructural change as well as cadmium content in the liver were studied by light and electron microscopies, atomic absorption spectroscopy and electron probe X-ray microanalyzer. Results showed that liver appeared to be one of the major target organs of cadmium poisoning, its cadmium contents in the experiment group were increased along with the successive treatment. Significant morphological changes were that the injury occured in almost all ultra-structures in the liver, including increase of glycogens, lysosomes and RER swelling of mitochondria. Destruction of disse space within the first two weeks; then followed by glycogens disappearance, RER dilatation, mitochondria destruction, collagerous fibers proliferation and partial cells dealth. After withdrawal of cadmium administration, the pathological processes were still in progress, finally terminated in cirrhosis. Cadmium microanalysis by electron probe X-ray microanalyzer revealed that there was no concentrated points and areas of Cd ions in the liver in this study, suggesting the possibility of binding cadmium to biomacromolccular substances.

关 键 词：镉中毒 肝损伤 病理学 亚慢性毒性 

分 类 号：R598.1[医药卫生—内科学]