Mercuric chloride‐induced kidney damage in mice: Time course and effect of dose

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Abstract
The rate of elimination of mercury after a single oral or intraperitoneal administration of HgCl2 to male or female mice has recently been demonstrated to be inversely related to the dose size (Nielsen and Andersen, 1989, 1990). The present study demonstrates dose‐related induction of renal tubular damage, followed by regeneration, after oral administration of HgCl2 to female mice. Dose‐related increased fractional urinary mercury excretion (expressed as percent of dose) was also demonstrated. At increasing dose of HgCl2, the renal activity of selenium‐dependent glutathione peroxidase decreased, and was only 50% of the activity in untreated controls after administration of 200 μmol HgCl2/kg. At higher doses, the renal concentration of glutathione was significantly reduced as well. The degree of tissue damage was inversely related to the fractional deposition of mercury in the kidneys. This study indicates that the reduction in fractional whole‐body retention of mercury with increasing dose size previously demonstrated is due to increased urinary mercury excretion during transient renal damage followed by regeneration, as extensive leakage took place before extensive regeneration was noted.