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Renal Na-S i cotransporter NaSi-1 is inhibited by heavy metals

1998; American Physical Society; Volume: 274; Issue: 2 Linguagem: Inglês

10.1152/ajprenal.1998.274.2.f283

1931-857X

Daniel Markovich, David Knight,

Renal and related cancers

Heavy metal intoxication leads to a number of reabsorptive and secretory defects in renal transport systems. We have studied the effects of several heavy metals on the expression of the renal Na-S i cotransporter NaSi-1. NaSi-1 cRNA was injected into Xenopusoocytes, and Na-S i cotransport activity was measured in the presence of mercury, lead, cadmium, or chromium. Mercury strongly inhibited NaSi-1 transport irreversibly by reducing both maximal velocity ( V max ) and Michaelis constant ( K m ) for inorganic sulfate (S i ). Lead inhibited NaSi-1 transport reversibly by decreasing V max but not K m for S i . Cadmium showed weak reversible inhibition of NaSi-1 transport by decreasing only NaSi-1 V max . Chromium strongly inhibited NaSi-1 cotransport reversibly by reducing K m for S i by sevenfold, most probably by binding to the S i site, due to the strong structural similarity between the C[Formula: see text] and[Formula: see text] substrates. In conclusion, this study presents an initial report demonstrating heavy metals inhibit renal brush border Na-S i cotransport via the NaSi-1 protein through various mechanisms and that this blockade may be responsible for sulfaturia following heavy metal intoxication.