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对小剂量氯化汞染毒大鼠肾小球进行了透射电镜的长期动态观察,见其超微结构改变的主要特点是内皮与基膜间、系膜区出现大量蛋白沉积物。肾小球基膜完整,亦未见上皮细胞有足突融合等表现,提示肾小球基膜并无结构性或负电性改变。研究认为血浆蛋白成分与Hg~(2+)结合后发生荷电性改变,可能是产生白蛋白尿及肾小球沉积物的主要原因,但并不排除此种沉积物可进而诱发肾小球免疫性损伤的可能性。本项研究为探索职业性汞性肾小球损伤机制提供了可靠模型。
The long-term dynamic observation of the glomerulus of rats exposed to a small dose of mercuric chloride shows that the main feature of the ultrastructural changes is the presence of a large amount of protein deposits in the mesangial area between the endothelium and the basement membrane. Glomerular basement membrane integrity, but also no epithelial cells have foot protrusion fusion performance, suggesting that there is no structural glomerular basement membrane or negative change. Study that the plasma protein composition and Hg ~ (2 +) combined with the occurrence of charge change, may be the main cause of albuminuria and glomerular deposits, but does not rule out this deposit can then induce glomerular Possibility of immune damage. This study provides a reliable model for exploring the mechanism of occupational mercury-induced glomerular injury.