Author(s): Simons TJ
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Abstract Zinc efflux from human red blood cells is largely brought about by a saturable mechanism that depends upon extracellular Ca2+ ions. It has a Vmax of about 35 mumol/10(13) cells hr, a Km for external Ca2+ of 1 x 10(-4) M, and a Km for internal Zn2+ of 1 x 10(-9) M. External Zn2+ inhibits with a K0.5 of 3 x 10(-6) M. Sr2+ is a substitute for external Ca2+, but changes in monovalent anions or cations have little effect on the Zn2+ efflux mechanism. It is unaffected by most inhibitors of red cell transport systems, although amiloride and D-600 (methoxyverapamil, a Ca2+ channel blocker) are weakly inhibitory. The transport is capable of bringing about the net efflux of Zn2+, against an electrochemical gradient, provided Ca2+ is present externally. This suggests it may be a Zn2+:Ca2+ exchange, which would be able to catalyze the uphill movement of Zn2+ at the expense of an inward Ca2+ gradient, which is itself maintained by the Ca2+ pump.
This article was published in J Membr Biol
and referenced in Pharmaceutica Analytica Acta