亚慢性镉中毒肾损伤的超微病理观察

Ultrastructural observation of subchronic cadmium-induced renal injury in rats.

研究表明:病变早期近曲小管上皮细胞线粒体肿胀、嵴减少或破裂,胞浆有较多细小空泡,溶酶体增多,并见“多泡膜层体”;随后近曲小管上皮坏死,多泡膜层体增多,刷状缘溃烂脱失,质膜皱褶破坏,核变形,肾小球内皮细胞、足细胞及远曲小管上皮细胞变性,病变后期胶原纤维广泛增生,肾硬化萎缩。肾皮质镉含量进行性升高,镉离子因与金属硫蛋白及其他金属结合蛋白结合,故电子探针X—线波谱扫描分析未见游离镉富集现象。

Male Wistar rats were treated with Cdcl_2 (5,3μmol Cd^(2+)/kg body wt., ip. 5 times a week up to 10 weeks). Dynamic observations of histological and ultrastructural morphometry were conducted by light and electron microscopy. Early significant ultrastructural alterations included swelling, decrease of cristae or rupture of mitochondria cytoplasmic edema with increased number of pinocytic vesicles and in some case, apical vesiculation, increase of small lysosomes and appearance of'mutivesicular lamellated body(MB)' etc, all in the cytoplasma in renal proximal tubular cells around the 2～4 week period of exposure; then followed by tubular necrosis in some area, darkening of cytoplasm, increase of MB, disappearance of organelle, appearance of a number of vesicles, festered brush border, destroy of the folder in plasmic membrance, change of nucleus shape and inclusion body in the nucleus. Moreover, degeneration of distal and collecting tubular cells, hypertrophy of glomerular epithelial cells thickening of the capsule and basal membrane; finally collagen fibers proliferated and terminated in cirrhosis. Cd concentrations in renal cortex were increased with the successive treatment and reached the highest plateaux at 9th week of exposue. Microanalysis of Cd by electron probe X-ray micro analyzer revealed that there wits no concentrated points or areas of Cd ions in the kidney tissue in this study, suggesting the possibility of binding of Cd to metalloproteins and other biomacromolecular substances.