| Abstract: | Renal Glutathione and Mercury Uptake by Kidney. BERNDT, W. O.,BAGGETT, J. MCC., BLACKER, A., AND HOUSER, M. (1985). Fundam.Appl. Toxicol.. 5,832-839. The kidney is well documented asthe target organ for mercuric ion. Mechanisms by which thision accumulates in renal tissue, however, are less well understood.Sulfhydryl groups in renal tissue might well bind this metaland serve as a sink for its accumulation. Various studies haveindicated that both methyl mercury as well as mercuric ion areaccumulated less by renal tissue after depletion of nonproteinsulfhydryl groups. A similar reduction in hepatic accumulationof mercuric ion or methyl mercury does not occur after nonproteinsulfhydryl depletion. This observation may relate to the highertissue content of nonprotein sulfhydryls in liver than kidneyor to a fundamentally different mechanism of metal uptake. Mercuricion accumulation by renal tissue also can be reduced by ureteralocclusion, a reduction that is less than that for inulin incomparable experiments. These data are complex and do not clearlyestablish a role for filtration in the delivery of mercury tothe kidney. Inhibition of the renal enzyme  glutamyl transpeptidase(-GT) results in a marked increase in the excretion of bothglutathione and mercury in the urine. Although there is a tendencyfor kidneys of the GT-inhibited animals to contain less mercurythan controls, the change in renal content was not significant.These observations suggest that -GT may have a role in the reabsorptionof mercury from the tubular lumen. Interestingly, both mercuricchloride-induced mortality and effects on renal slice accumulationof organic ions were enhanced in the presence of nonproteinsulfhydryl depletion caused both by immediate depletion of theglutathione pool and by inhibition of its synthesis. |
