Abstract
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 HgCl 2 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 HgCl 2 injection substantially reduced renal Hg content and consequently reduced the renal damage. In addition, coadministration of GSH (36 μmol/kg, i.v.) with HgCl 2 increased the renal Hg content measured 5 min after HgCl 2 injection to 2.6 fold higher than that of mice treated with HgCl 2 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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.