Nonhepatic thioacetamide injury. II. The morphologic features of proximal renal tubular injury.
Thioacetamide given orally to rats produces centrolobular hepatic necrosis and also causes death of the cells in the terminal portion of the proximal renal tubule. The morphologic changes observed during the course of the renal toxicity include the early and transient appearance of apical dense bodies, which appear to fuse to form large lysosomes, and the appearance of nucleolar hypertrophy, reminiscent of the same change seen in the hepatocytes. In addition a variety of changes described in lethally injured tubular cells in other toxicities appear. A diuresis, which lasts for 5 days, coincides with the appearance of tubular cell destruction. The mechanism of cell injury due to thioacetamide is not identified, but the temporal sequence of morphologic and physiologic change is consistent with both a relative concentration of the thioacetamide in the proximal tubule and its potential conversion to a putative proximate toxin.
D000081:Acetamides / Q000633:toxicity*; D000818:Animals; D002466:Cell Nucleolus; D056486:Chemical and Drug Induced Liver Injury / Q000473:pathology*; D004231:Diuresis / Q000187:drug effects; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology; D007687:Kidney Tubules, Proximal / Q000187:drug effects* / Q000473:pathology; D008247:Lysosomes; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D013853:Thioacetamide / Q000378:metabolism / Q000633:toxicity
D000081:Acetamides; D013853:Thioacetamide