Abstract

Indium chloride, a nephrotoxic and porphyrogenic chemical, exerts a tissue-specific inhibition of δ-aminolevulinic acid (ALA) dehydratase in rat kidney. This effect appears to be related to the preferential accumulation of indium by the kidney proximal tubule cell and to the selective localization of indium within the cytosolic fraction of that cell type, as assessed by electron microscopy. The reversal of indium-induced inhibition of renal ALA dehydratase both in vivo and in vitro by zinc suggests that indium acts by binding with sulfhydryl groups of the enzyme. The synergistic effects of lead and indium with respect to inhibition of renal ALA dehydratase suggest that exposure to weak sulfhydryl inhibitors such as the group III metals may enhance the renal toxicity of other metals which may not in themselves exert overt toxic effects in that organ.

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