The effects of palmitic acid (PA) and the products of its ω-oxidation–ω-hydroxypalmitic acid (HPA) and α,ω-hexadecanedioic acid (HDA)—on respiration in the absence of ATP synthesis and on the H2O2 generation were studied on isolated liver mitochondria energized by oxidation of succinate. It was shown that HPA stimulates respiration and reduces the difference in electrical potentials (Δψ) in mitochondria to the same extent as is typical for PA and classical protonophore uncouplers. Under similar conditions, the stimulation of mitochondrial respiration by HDA is not accompanied by a decrease in Δψ and is suppressed by 10 μM cyclosporin A. In this regard, HDA is considered as a “decoupling” agent that switches the complexes of the mitochondrial respiratory chain to the idle mode. It was established that in the presence of 20 mM potassium chloride in the sucrose incubation medium, stimulation of respiration by HPA (in contrast to PA and HDA) is suppressed by 60% in the case of pre-incubation with 3 mM magnesium chloride. We found that under these conditions, HPA at a concentration of 25 μM and above induces mitochondrial swelling, which is completely suppressed by magnesium chloride. HPA as an inducer of mitochondrial swelling is less efficient in the absence of potassium chloride than in its presence. We assume that, in contrast to PA and HDA, HPA produces its activating influence on free respiration in mitochondria owing to a combination of its ionophore and protonophore effects. It was established that PA, HDA, and HPA in concentrations equally stimulating respiration of mitochondria in state 2 are equally efficient in inhibiting the H2O2 generation. We conclude that the effects of these fatty acids as inhibitors of H2O2 generation in isolated liver mitochondria are due to stimulation of respiration in various ways and are not associated with a decrease in Δψ.

中文翻译：

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ω-羟基棕榈酸和 α,ω-十六烷二酸作为肝脏线粒体中自由呼吸的激活剂和 H2O2 生成的抑制剂

研究了棕榈酸 (PA) 及其 ω-氧化-ω-羟基棕榈酸 (HPA) 和 α,ω-十六烷二酸 (HDA) 的产物——在没有 ATP 合成的情况下对呼吸和 H2O2 生成的影响在通过琥珀酸氧化激活的分离的肝线粒体上。结果表明，HPA 刺激呼吸并减少线粒体中的电位差 (Δψ)，其程度与 PA 和经典质子细胞解偶联剂的典型程度相同。在类似条件下，HDA 对线粒体呼吸的刺激不伴随 Δψ 的降低，而是被 10 μM 环孢菌素 A 抑制。 在这方面，HDA 被认为是一种“解偶联”剂，可以切换线粒体呼吸链的复合物进入空闲模式。已经确定，在蔗糖培养介质中存在 20 mM 氯化钾时，在用 3 mM 氯化镁预培养的情况下，HPA（与 PA 和 HDA 相比）对呼吸的刺激被抑制了 60%。我们发现在这些条件下，浓度为 25 μM 及以上的 HPA 会诱导线粒体肿胀，而这完全被氯化镁抑制。HPA 作为线粒体肿胀的诱导剂在没有氯化钾的情况下比在氯化钾存在的情况下效率低。我们假设，与 PA 和 HDA 相比，HPA 由于其离子载体和质子载体效应的结合，对线粒体中的自由呼吸产生激活影响。已确定 PA、HDA、和 HPA 的浓度同样刺激状态 2 中的线粒体呼吸在抑制 H2O2 生成方面同样有效。我们得出结论，这些脂肪酸作为分离肝线粒体中 H2O2 生成的抑制剂的作用是由于以各种方式刺激呼吸，与 Δψ 的降低无关。