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首页> 外文期刊>American Journal of Physiology >Renal Na-Si cotransporter NaSi-1 is inhibited by heavy metals.
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Renal Na-Si cotransporter NaSi-1 is inhibited by heavy metals.

机译：肾脏Na-Si共转运体NaSi-1被重金属抑制。

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摘要

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-Si cotransporter NaSi-1. NaSi-1 cRNA was injected into Xenopus oocytes, and Na-Si 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 (Vmax) and Michaelis constant (Km) for inorganic sulfate (Si). Lead inhibited NaSi-1 transport reversibly by decreasing Vmax but not Km for Si. Cadmium showed weak reversible inhibition of NaSi-1 transport by decreasing only NaSi-1 Vmax. Chromium strongly inhibited NaSi-1 cotransport reversibly by reducing Km for Si by sevenfold, most probably by binding to the Si site, due to the strong structural similarity between the CrO4(2-) and SO4(2-) substrates. In conclusion, this study presents an initial report demonstrating heavy metals inhibit renal brush border Na-Si cotransport via the NaSi-1 protein through various mechanisms and that this blockade may be responsible for sulfaturia following heavy metal intoxication.
机译：重金属中毒会导致肾脏转运系统出现许多吸收和分泌缺陷。我们已经研究了几种重金属对肾Na-Si共转运蛋白NaSi-1表达的影响。将NaSi-1 cRNA注射到非洲爪蟾卵母细胞中，并在汞，铅，镉或铬存在下测量Na-Si共转运活性。汞通过降低无机硫酸盐（Si）的最大速度（Vmax）和米氏常数（Km）来不可逆地强烈抑制NaSi-1的运输。铅通过降低Vmax而可逆地抑制NaSi-1的迁移，但不降低Km的Si。镉通过仅降低NaSi-1 Vmax表现出对NaSi-1转运的弱可逆抑制作用。由于CrO4（2-）和SO4（2-）底物之间的强烈结构相似性，铬通过将Si的Km降低7倍（最可能是通过与Si位置结合）来强烈可逆地抑制NaSi-1共转运。总之，这项研究提供了一份初步报告，表明重金属通过各种机制通过NaSi-1蛋白抑制了肾刷状边界Na-Si共转运，并且这种阻断作用可能是重金属中毒后引起的血尿过多的原因。

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