Role of renal cortical sulfhydryl groups in development of mercury‐induced renal toxicity

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Abstract
The effect of lowering renal cortical SH concentration on development of acute renal failure (ARF) was evaluated in rats receiving HgCl2 (15 mg/kg body wt, i.m.). Within 90 min after HgCl2 injection, urine flow rate and fractional excretion of Na (FENa) were significantly elevated above control levels, and they remained elevated throughout the 3-h experimental period. Urine flow rate and FENa were not significantly elevated above control levels in animals injected with diethyl maleate (3 mmol/kg, i.p.) 30 min before and 90 min after HgCl2 (DEM/HgCl2). Administration of DEM alone did not alter renal function. Although lower than control levels, concentrations of protein-bound SH groups (PBSH) were comparable in HgCl2- and DEM/HgCl2-treated animals. Concentrations of nonprotein SH groups (NPSH) were 62% lower in DEM/HgCl2 animals than in those treated with HgCl2 alone. Hg accumulation was 54% lower in DEM/HgCl2-treated animals than in animals treated with HgCl2 alone. Apparently, HPSH played an important role in uptake and development of Hg toxicity.