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癸基泛醌可增加突触体中线粒体的功能。

Decylubiquinone increases mitochondrial function in synaptosomes.

机构信息

School of Biochemistry and Immunology and Trinity College Institute of Neuroscience, Trinity College, Dublin 2, Ireland.

出版信息

J Biol Chem. 2010 Mar 19;285(12):8639-45. doi: 10.1074/jbc.M109.079780. Epub 2010 Jan 14.

Abstract

The effects of decylubiquinone, a ubiquinone analogue, on mitochondrial function and inhibition thresholds of the electron transport chain enzyme complexes in synaptosomes were investigated. Decylubiquinone increased complex I/III and complex II/III activities by 64 and 80%, respectively, and attenuated reductions in oxygen consumption at high concentrations of the complex III inhibitor myxothiazol. During inhibition of complex I, decylubiquinone attenuated reductions in synaptosomal oxygen respiration rates, as seen in the complex I inhibition threshold. Decylubiquinone increased the inhibition thresholds of complex I/III, complex II/III, and complex III over oxygen consumption in the nerve terminal by 25-50%, when myxothiazol was used to inhibit complex III. These results imply that decylubiquinone increases mitochondrial function in the nerve terminal during complex I or III inhibition. The potential benefits of decylubiquinone in diseases where complex I, I/III, II/III, or III activities are deficient are discussed.

摘要

研究了癸基泛醌(一种泛醌类似物)对突触体中线粒体功能和电子传递链酶复合物抑制阈值的影响。癸基泛醌分别使复合物 I/III 和复合物 II/III 的活性增加了 64%和 80%,并减弱了复合物 III 抑制剂鱼藤酮高浓度时对耗氧量的降低作用。在复合物 I 受到抑制时,癸基泛醌减弱了如在复合物 I 抑制阈值中所见的突触体氧呼吸速率的降低。癸基泛醌增加了复合物 I/III、复合物 II/III 和复合物 III 在神经末梢的抑制阈值,与复合物 III 抑制剂鱼藤酮抑制复合物 III 时相比,耗氧量增加了 25-50%。这些结果表明,在复合物 I 或 III 受到抑制时,癸基泛醌增加了神经末梢中线粒体的功能。讨论了癸基泛醌在复合物 I、I/III、II/III 或 III 活性缺乏的疾病中的潜在益处。

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