摘要：Mercuric chloride is a well-known human and animal nephrotoxicant. Previous studies have demonstrated an inverse relationship between dose size and relative whole-body retention of mercury after oral administration of mercuric chloride to mice. The present study indicates that this inverse relationship is caused by a dose-related induction of kidney damage leading to increasing leakage of mercury through the kidneys. Histopathologic investigation revealed extensive necrosis of the proximal tubules in kidneys from mice exposed to 100 mumole HgCl2/kg or higher doses. Moreover, maximum renal damage occurred between days 2 and 3 after administration. The renal damage was followed by regeneration, which was observed between days 3 and 7 at increasing dose levels up to 100 mumole HgCl2/kg. The amount of glutathione and the glutathione peroxidase activity in kidney decreased with increasing doses of mercuric chloride. The reduced glutathione peroxidase activity was due to a reduction in selenium-dependent glutathione peroxidase activity. The level of lipid peroxidation was not changed by increasing doses of mercuric chloride, and hence was not a primary toxic mechanism in acute nephrotoxicity induced by mercuric chloride. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (689K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . 317 318 319 320
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