嗜盐菌亚细菌颗粒中的光驱动钠运输。

Light-driven sodium transport in sub-bacterial particles of Halobacterium halobium.

作者信息

Eisenbach M, Cooper S, Garty H, Johnstone R M, Rottenberg H, Caplan S R

出版信息

Biochim Biophys Acta. 1977 Mar 17;465(3):599-613. doi: 10.1016/0005-2736(77)90276-0.

Abstract

Light-induced Na+ efflux was observed in sub-bacterial particles of Halobacterium halobium loaded and suspended in 4 M NaCl solution. The Na+ efflux was not ATP driven, since ATPase inhibitors were without effect or even enhanced efflux at low light intensity. Uncouplers, on the other hand, inhibited Na+ efflux, the inhibition being complete at low light intensity. The Na+ efflux was accompanied by proton influx. Both processes were dependent on light intensity, unaffected or enhanced by ATPase inhibitors and similarly affected by uncouplers. Proton influx was not observed in particles loaded with 4 M KCl instead of 4 M NaCl. Na+ transport in the dark could be induced by artificial formation of a pH difference across the membrane; changing the sign of the pH difference reversed the direction of the Na+ transport. Proton influx in the dark followed the artificial formation of a sodium gradient [Na+]in less than [Na+]out). These results may be explained by a Na+/H+ antiport mechanism. The fluxes of Na+ and H+ were of comparable magnitude, but the initial rate of Cl- efflux in the same experiment was one-third of the initial rate of Na+ efflux. Consequently Cl- is not regarded as a participant in the Na+ efflux mechanism.

摘要

在加载并悬浮于4M NaCl溶液中的嗜盐菌亚细菌颗粒中观察到光诱导的Na⁺外流。这种Na⁺外流不是由ATP驱动的，因为ATP酶抑制剂没有作用，甚至在低光强度下还会增强外流。另一方面，解偶联剂抑制Na⁺外流，在低光强度下抑制作用完全。Na⁺外流伴随着质子内流。这两个过程都依赖于光强度，不受ATP酶抑制剂的影响或增强，并且同样受到解偶联剂的影响。在加载4M KCl而非4M NaCl的颗粒中未观察到质子内流。黑暗中的Na⁺运输可通过人工在膜两侧形成pH差异来诱导；改变pH差异的符号会逆转Na⁺运输的方向。黑暗中的质子内流跟随人工形成的钠梯度（[Na⁺]内小于[Na⁺]外）。这些结果可以用Na⁺/H⁺反向转运机制来解释。Na⁺和H⁺的通量大小相当，但在同一实验中，Cl⁻外流的初始速率是Na⁺外流初始速率的三分之一。因此，Cl⁻不被视为Na⁺外流机制的参与者。