Simons T J
Biomedical Sciences Division, King's College London, Strand.
J Membr Biol. 1991 Jul;123(1):73-82. doi: 10.1007/BF01993965.
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.
人体红细胞中的锌外流主要由一种依赖细胞外钙离子的可饱和机制引起。其最大反应速度约为35 μmol/10¹³个细胞·小时，细胞外钙离子的米氏常数为1×10⁻⁴ M，细胞内锌离子的米氏常数为1×10⁻⁹ M。细胞外锌离子的抑制常数为3×10⁻⁶ M。锶离子可替代细胞外钙离子，但单价阴离子或阳离子的变化对锌离子外流机制影响很小。尽管氨氯吡咪和D - 600（甲氧基维拉帕米，一种钙离子通道阻滞剂）有微弱抑制作用，但它不受大多数红细胞转运系统抑制剂的影响。只要细胞外存在钙离子，这种转运就能逆着电化学梯度实现锌离子的净外流。这表明它可能是一种锌离子：钙离子交换，能够以向内的钙离子梯度为代价催化锌离子的上坡运动，而钙离子梯度本身由钙离子泵维持。
