Theoretical and experimental studies have revealed that that in the liver mitochondria an increase in the rate of free respiration in state 3 induced by protonophore uncouplers 2,4-dinitrophenol and сarbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone is equal to or slightly greater than the increase in respiration rate in state 4 induced by these uncouplers. In contrast to these protonophore uncouplers, the decoupler α,ω-tetradecanedioic acid, increasing the rate of respiration in state 4, does not significantly affect the rate of free respiration in state 3. We have proposed quantitative indicators that allow determining the constituent part of the rate of respiration in state 4, associated with the decoupling effect of the uncoupler. Using the example of palmitic acid, we have found out the fundamental possibility of the simultaneous functioning of uncouplers by two mechanisms: as protonophores and as decouplers. The data obtained contradict the delocalized version of Mitchell’s chemiosmotic theory, but are in complete agreement with its local version. It can be assumed that the F₀F₁-ATP synthase and nearby respiratory chain complexes form a local zone of coupled respiration and oxidative ATP synthesis (zones of oxidative phosphorylation). The uncoupler-induced stimulation of mitochondrial free respiration of mitochondria in state 3 is mainly due to the return of protons to the matrix in local zones, where the generation of a proton motive force (Δр) by respiratory chain complexes is associated with various transport processes, but not with ATP synthesis (zones of protonophore uncoupling). In contrast, respiratory stimulation in state 4 by decouplers is realized in local zones of oxidative phosphorylation by switching the respiratory chain complexes to the idle mode of operation in the absence of ATP synthesis.

中文翻译：

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质子细胞解偶联剂和解偶联剂在状态 3 和 4 中作为线粒体自由呼吸诱导剂作用的比较研究：理论和实验方法。

理论和实验研究表明，在肝脏线粒体中，由质子体解偶联剂 2,4-二硝基苯酚和 羰基氰 4-(三氟甲氧基)苯腙诱导的状态 3 自由呼吸速率的增加等于或略大于增加由这些解偶联剂引起的状态 4 的呼吸速率。与这些质子细胞解偶联剂相比，解偶联剂 α,ω-十四烷二酸增加了状态 4 的呼吸速率，不会显着影响状态 3 的自由呼吸速率。 我们提出了定量指标，可以确定状态 4 中的呼吸速率，与解耦器的解耦效应相关。以棕榈酸为例，我们已经发现解偶联剂通过两种机制同时发挥作用的基本可能性：作为质子载体和作为解偶联剂。获得的数据与米切尔化学渗透理论的离域版本相矛盾，但与其局部版本完全一致。可以假设F ₀ F ₁ -ATP 合酶和附近的呼吸链复合物形成耦合呼吸和氧化 ATP 合成的局部区域（氧化磷酸化区域）。解偶联剂对状态 3 线粒体自由呼吸的刺激主要是由于质子返回到局部区域的基质，其中呼吸链复合物产生的质子动力 (Δ р ) 与各种运输有关过程，但不是 ATP 合成（质子细胞解偶联区）。相比之下，在没有 ATP 合成的情况下，通过将呼吸链复合物切换到空闲操作模式，在氧化磷酸化的局部区域中实现了解耦剂在状态 4 中的呼吸刺激。