Barker E A, Smuckler E A
Am J Pathol. 1974 Mar;74(3):575-90.
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.
给大鼠口服硫代乙酰胺会导致肝小叶中央坏死,还会引起近端肾小管末端细胞死亡。在肾脏毒性过程中观察到的形态学变化包括顶端致密小体早期短暂出现,这些致密小体似乎融合形成大的溶酶体,以及核仁肥大的出现,这让人联想到在肝细胞中看到的相同变化。此外,还出现了在其他毒性中描述的致死性损伤肾小管细胞的各种变化。持续5天的多尿与肾小管细胞破坏的出现同时发生。硫代乙酰胺导致细胞损伤的机制尚未明确,但形态学和生理学变化的时间顺序与硫代乙酰胺在近端小管中的相对浓度及其潜在转化为假定的直接毒素均相符。