PMID: 8948017Oct 1, 1996Paper

Nephrotoxicity of thioformamide, a proximate toxicant of nephrotoxic thiazoles, in mice depleted of glutathione

Research Communications in Molecular Pathology and Pharmacology
T MizutaniK Nakanishi

Abstract

Administration of thioformamide (TFA) (> 2 mmol/kg, sc) in combination with DL-buthionine sulfoximine (BSO) (4 mmol/kg, i.p.), an inhibitor of glutathione (GSH) synthesis, caused kidney injury in male mice. The injury was characterized by tubular necrosis, increases in relative kidney weight and serum urea nitrogen concentration, and a decrease in renal GSH concentration. In contrast to results in male mice, no overt nephrotoxic effects were observed in female mice given TFA in combination with BSO. These features of nephrotoxicity were very similar to those reported for thiabendazole and other nephrotoxic thiazoles in mice depleted of GSH by treatment with BSO; this resemblance supports the suggestion that TFA as a ring cleavage metabolite, or a further metabolite thereof, is responsible for the toxicity of the nephrotoxic thiazoles (Mizutani, T., Yoshida, K., and Kawazoe, S. (1993) Chem. Res. Toxicol. 6, 174-179).

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