Jung D W, Farooqui T, Utz E, Brierley G P
J Bioenerg Biomembr. 1984 Dec;16(5-6):379-90. doi: 10.1007/BF00743233.
Quinine inhibits the respiration-dependent extrusion of K+ from Mg2+-depleted heart mitochondria and the passive osmotic swelling of these mitochondria in K+ and Na+ acetate at alkaline pH. These observations concur with those of Nakashima and Garlid (J. Biol. Chem. 257, 9252, 1982) using rat liver mitochondria. Quinine also inhibits the respiration-dependent contraction of heart mitochondria swollen passively in Na+ or K+ nitrate and the increment of elevated respiration associated with the extrusion of ions from these mitochondria. Quinine, at concentrations up to 0.5 mM, inhibits the respiration-dependent 42K+/K+ exchange seen in the presence of mersalyl, but higher levels of the drug produce increased membrane permeability and net K+ loss from the matrix. These results are all consistent with an inhibition of the putative mitochondrial K+/H+ antiport by quinine. However, quinine has other effects on the mitochondrial membrane, and possible alternatives to this interpretation are discussed.
奎宁抑制了K⁺从Mg²⁺缺乏的心脏线粒体中通过呼吸作用的排出,以及这些线粒体在碱性pH值下于K⁺和乙酸钠中发生的被动渗透性肿胀。这些观察结果与中岛和加利多(《生物化学杂志》257, 9252, 1982)使用大鼠肝脏线粒体的观察结果一致。奎宁还抑制了在硝酸钠或硝酸钾中被动肿胀的心脏线粒体的呼吸依赖性收缩,以及与这些线粒体中离子排出相关的呼吸增强。浓度高达0.5 mM的奎宁抑制了在汞撒利存在下观察到的呼吸依赖性42K⁺/K⁺交换,但更高浓度的该药物会导致膜通透性增加以及基质中K⁺净流失。这些结果均与奎宁对假定的线粒体K⁺/H⁺反向转运体的抑制作用一致。然而,奎宁对线粒体膜还有其他影响,本文讨论了对此解释的可能替代方案。