The subcellular distribution and ultrastructural effects of lead have been studied in the kidneys and liver of rats given lead acetate (600 ppm Pb 2+) in their drinking water for 6 months. Control rats were given sodium acetate. Tissue samples were fixed in glutaraldehyde and examined by electron microscopy with and without staining. Unstained sections of both kindey and liver from lead-treated animals showed small particles (2-5 nm diameter) of very high electron density which appear to represent a deposited form of Pb 2+. Ultrastructural changes in the kidneys were largely confined to glomeruli (swelling of endothelial cells, fusion of foot processes, thickening of basement membrane) and proximal tubules (ranging from minimal sub-lethal changes to necrotic disorganization). The electron-dense particles of Pb 2+ occurred in large clusters in basement membranes. As individual particles, or small groups, they were numerous in nuclei of proximal epithelium but usually only a few, largely confined to vesicles or inclusion bodies, were present in the cytoplasm. Only when cells were markedly damaged morphologically were particles more generally distributed in the cytoplasm. Liver damage by Pb 2+ was largely confined to centrilobular regions. Endothelial and Kupffer cells were the most affected; they often sequestered large numbers of the particles. In parenchymal cells, particles were few and mainly in vesicles, but they were more widely distributed in the cytoplasm when morphological injury was apparent. The free distribution of Pb 2+ in liver and kidney seems to be limited by its deposition in basement membranes and sequestration in reticulo-endothelial cells; intracellular distribution in healthy cells is also limited, by deposition in nuclei (in kidney only) or cytoplasmic vesicles.
|Number of pages||14|
|Journal||British Journal of Experimental Pathology|
|Publication status||Published - 1988|
ASJC Scopus subject areas
- Pathology and Forensic Medicine