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[线粒体膜双层电层间质子转运的控制]

[Control of proton transport across the double electrical layers of mitochondrial membranes].

作者信息

Dragunova S F, Krasinskaia I P, Iaguzhinskiĭ L S

出版信息

Biokhimiia. 1981 Jun;46(6):1087-95.

PMID:7260195
Abstract

The effects of cardiolipin, dodecylsulfate anion and K+ on inhibition of respiration of intact and briefly frozen mitochondria by electrophylic compounds, e. g. beta-haloidalkylamines-p-(N,N-di-2-chlorethylamino)phenylacetic (I) and--phenylbutyric (II) acids were studied. It was shown that in K+-containing media the increase of the negative surface charge of the frozen mitochondrial membrane enhances the inhibition of mitochondrial respiration. In media without K+ this affect is absent. The inhibition of mitochondrial respiration by I and II is due to local increase of activity of the acids in mitochondrial membrane in the course of hydrolysis. It was assumed that the double electrical layers hamper the transport of the acid from the hydrophobic zone of the membrane into the environment including the water phase. Using this model, it was demonstrated that when the double electrical layer is destroyed, the inhibition of respiration by I is decreased at increased buffer capacity of the incubation medium. Correspondingly, in intact mitochondria the buffer capacity of the medium does not practically affect the inhibition of respiration by I.

摘要

研究了心磷脂、十二烷基硫酸根阴离子和K⁺对亲电化合物(如β-卤代烷基胺 - 对 -(N,N - 二 - 2 - 氯乙基氨基)苯乙酸(I)和对 - 苯基丁酸(II))抑制完整和短暂冷冻线粒体呼吸作用的影响。结果表明,在含K⁺的介质中,冷冻线粒体膜负表面电荷的增加增强了对线粒体呼吸的抑制作用。在不含K⁺的介质中则不存在这种影响。I和II对线粒体呼吸的抑制作用是由于在水解过程中线粒体膜中酸的活性局部增加所致。据推测,双电层阻碍了酸从膜的疏水区域转运到包括水相在内的环境中。利用该模型证明,当双电层被破坏时,在孵育介质缓冲容量增加的情况下,I对呼吸的抑制作用降低。相应地,在完整线粒体中,介质的缓冲容量实际上并不影响I对呼吸的抑制作用。

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