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In vivo nephrotoxicity induced in mice by chromium(VI)

Involvement of glutathione and chromium(V)

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Abstract

The role of glutathione (GSH) and chromium (V) in chromium (VI)-induced nephrotoxicity in mice was investigated at 24 h after K2Cr(VI)2O7 ip injection. Nephrotoxicity was assessed by measurements of relative kidney weight and serum urea nitrogen. Cr(VI) nephrotoxicity was accompanied by decreased renal GSH and glutathione reductase (GSSG-R) levels. Pretreatment with buthionine sulfoximine, an inhibitor of GSH biosynthesis, enhanced Cr(VI)-induced nephrotoxicity, and remarkably diminished kidney GSH and GSSG-R levels. In contrast, pretreatment with glutathione methyl ester, a GSH-supplying agent, prevented Cr(VI) from exerting a harmful effect on mouse kidney and restored kidney GSH level. Administration of a Cr(V) compound, K3Cr(V)O8, induced much higher toxicity in mouse kidney than Cr(VI), but it failed to diminish renal GSH level. Another Cr(V) compound, Cr(V)-GSH complex, and Cr(III) nitrate did not cause a nephrotoxic effect in mice. The mechanism of Cr(VI)-induced nephrotoxicity was explained using GSH and Cr(V).

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Authors and Affiliations

  1. Laboratory of Environmental Health and Toxicology, Department of Food Science and Nutrition, Kyoto Prefectural University, 606, Shimogamo, Kyoto, Japan

    Yasuji Hojo & Yoshiko Satomi

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  1. Yasuji Hojo
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  2. Yoshiko Satomi
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Hojo, Y., Satomi, Y. In vivo nephrotoxicity induced in mice by chromium(VI). Biol Trace Elem Res 31, 21–31 (1991). https://doi.org/10.1007/BF02990356

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  • DOI: https://doi.org/10.1007/BF02990356

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