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  • Artikel: DFG Deutsche Nationallizenzen  (2)
  • Mouse  (1)
  • Renal transport  (1)
  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Archives of toxicology 63 (1989), S. 479-483 
    ISSN: 1432-0738
    Schlagwort(e): Mercury metabolism ; Glutathione ; Detoxication ; Renal transport
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract To elucidate the mechanism by which methylmercury (MeHg) is eliminated from organisms, male C57BL/6N mice were orally administered with MeHg chloride (5 mg/kg) and the chemical forms of its metabolites in plasma, urine and the kidney were determined by column chromatographic analysis. Orally administered MeHg rapidly entered the circulation, accumulated in the kidney and other tissues, and was slowly excreted in the urine. Ultrafiltration and gel filtration analysis revealed that most of plasma MeHg was accounted for by its albumin conjugate. Cell fractionation analysis revealed that about 80% of renal MeHg was recovered from the 15 000 g supernatant fraction of the kidney homogenate. If the kidney was homogenized in the presence of serine-borate complex, a potent inhibitor of γ-glutamyltranspeptidase (γ-GTP), about 50% of the MeHg in the supernatant fraction was recovered as its glutathione S-conjugate while the rest was bound to cytosolic protein(s). The major part of urinary MeHg was accounted for by its cysteine conjugate. However, urinary excretion of its glutathione conjugate increased significantly if animals were pretreated with acivicin, an affinity labeling reagent for γ-GTP. These and other results suggested that MeHg bound to albumin accumulated in the kidney predominantly via some non-filtrating peritubular mechanism, and localized in renal cytosolic compartment as its glutathione- and protein-bound forms. The glutathione S-conjugate of MeHg in the tubule cells might be transferred to the lumenal space, hydrolyzed to the cysteine S-conjugate, and then excreted in urine. These sequential events might constitute an important eliminatory pathway for a hazardous mercurial metabolite in mice.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Archives of toxicology 59 (1986), S. 99-102 
    ISSN: 1432-0738
    Schlagwort(e): Methylmercury ; Excretion ; Distribution ; Strain difference ; Mouse
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract The strain differences in mercury excretion and organ distribution after administration of methylmercuric chloride (5 mg/kg) were studied in male mice of four strains, C57BL/6N, BALB/cA, C3H/HeN and AKR. The urinary excretion rate of mercury for 5 days following administration was 3.9–4.7 times higher in the C57BL strain than in the other three strains, whereas the mercury level in feces was highest in the AKR strain. Although the blood mercury concentration in the C57BL strain was almost half that in the others up to the 5th day, the plasma levels did not vary so widely. C57BL showed the highest ratio of plasma to whole blood mercury level, which was thought to originate from the lower affinity of methylmercury for hemoglobin. The variation of the plasma/whole blood ratios was rather small throughout the experimental period in each strain examined. In the C57BL strain, the mercury levels in brain, liver, kidney and blood were significantly lower on and after the 5th day than in the other three strains, probably because of the rapid elimination of body mercury into urine, but the mercury uptake by the brain and kidney 5 min after administration was at a rather higher rate than in the other strains. On the other hand, the highest tissue levels were shown by the C3H strain in the brain and liver, and by the BALB/c strain in the kidney. It was suggested that in the C57BL strain, the higher mercury distribution in plasma and rapid uptake by the kidney might result in higher urinary excretion.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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