Calcium-dependent zinc efflux in human red blood cells

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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 aV max of about 35 μmol/1013 cells hr, aK m for external Ca2+ of 1×10−4 m, and aK m for internal Zn2+ of 1×10−9 m. External Zn2+ inhibits with aK 0.5 of 3×10−6 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 it self maintained by the Ca2+ pump.