Role of γ-glutamyltranspeptidase in renal uptake and toxicity of inorganic mercury in mice

Toshiko Tanaka, Akira Naganuma, Nobumasa Imura

研究成果: Article査読

75 被引用数 (Scopus)

抄録

The role of renal glutathione (GSH) metabolism as a mediating factor in the renal uptake and toxicity of inorganic mercury was investigated in mice by preadministering a γ-glutamyltranspeptidase (GGT) inhibitor, acivicin. Pretreatment with acivicin (0.25, 1.0 or 2.5 mmol/kg, i.p.) led to a dose-dependent decrease in renal mercury content and increases in mercury and GSH contents in urine measured 2 h after HgCl2 injection (18 μmol/kg, i.v.). Acivicin pretreatment also ameliorated the renal and lethal toxicity caused by administration of inorganic mercury. Treatment of the mice with 1,2-dichloro-4-nitrobenzene (DCNB, 2.5 mmol/kg, i.p.), a specific depletor of hepatic GSH, prior to HgCl2 injection substantially reduced renal Hg content and consequently reduced the renal damage. In addition, coadministration of GSH (36 μmol/kg, i.v.) with HgCl2 increased the renal Hg content measured 5 min after HgCl2 injection to 2.6 fold higher than that of mice treated with HgCl2 alone. These results suggest that renal uptake of inorganic mercury, which is supposedly transported to the kidney as a mercury-GSH complex, is dependent on a reaction catalyzed by GGT on the outer surface of the renal brush border membrane in the same manner as the metabolism of GSH.

本文言語English
ページ(範囲)187-198
ページ数12
ジャーナルToxicology
60
3
DOI
出版ステータスPublished - 1990 3 16

ASJC Scopus subject areas

  • 毒物学

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