Smith T C, Levinson C
J Membr Biol. 1975;23(3-4):349-65. doi: 10.1007/BF01870257.
The membrane potential of Ehrlich ascites tumor cells and the effects of valinomycin and ouabain upon it have been determined. The membrane potential in control cells was 12.0 mV, inside negative. Neither valinomycin nor ouabain alone affected this value. However, valinomycin and ouabain in combination resulted in a slight hyperpolarization of the membrane. Concomitant determinations of cellular Na+, K+ and Cl- showed that valinomycin induced net losses of K+ and Cl- and a net gain in Na+ when compared to ouabain-inhibited cells. K+ permeability was increased by approximately 30% in the presence of valinomycin. In addition, valinomycin caused a rapid depletion of cellular ATP. Inhibition of Na/K transport by ouabain was without sparing effect on the rate of ATP depletion. Possible mechanisms for the electroneutral increase in K+ permeability induced by valinomycin are discussed.
已测定艾氏腹水癌细胞的膜电位以及缬氨霉素和哇巴因对其的影响。对照细胞的膜电位为12.0 mV，内负外正。单独使用缬氨霉素或哇巴因均未影响该值。然而，缬氨霉素和哇巴因联合使用导致膜轻微超极化。对细胞内Na⁺、K⁺和Cl⁻的同步测定表明，与哇巴因抑制的细胞相比，缬氨霉素导致K⁺和Cl⁻净损失以及Na⁺净增加。在缬氨霉素存在的情况下，K⁺通透性增加了约30%。此外，缬氨霉素导致细胞ATP迅速消耗。哇巴因对Na⁺/K⁺转运的抑制对ATP消耗速率没有节省作用。讨论了缬氨霉素诱导K⁺通透性电中性增加的可能机制。
