In vivo nephrotoxicity induced in mice by chromium(VI) View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1991-10

AUTHORS

Yasuji Hojo, Yoshiko Satomi

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). More... »

PAGES

21-31

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf02990356

DOI

http://dx.doi.org/10.1007/bf02990356

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027894577

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/1724173


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