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人类线粒体变体对氧气消耗的影响。

Human mitochondrial variants influence on oxygen consumption.

作者信息

Marcuello Ana, Martínez-Redondo Diana, Dahmani Yahya, Casajús José A, Ruiz-Pesini Eduardo, Montoya Julio, López-Pérez Manuel J, Díez-Sánchez Carmen

机构信息

Departmento de Bioquímica y Biología Molecular y Celular, Universidad de Zaragoza, Miguel Servet 177, 50013 Zaragoza, Spain.

出版信息

Mitochondrion. 2009 Feb;9(1):27-30. doi: 10.1016/j.mito.2008.10.002. Epub 2008 Oct 15.

Abstract

This work investigates if human mitochondrial variants influence on maximal oxygen consumption (VO(2max)). With this purpose we recruited, as a uniform population in term of nutritional habits and life style, 114 healthy male Spanish subjects that practiced fitness exercises 3-4 times a week. Once mtDNA haplogroups were determined, we found that J presents with lower VO(2max) (P=0.02) than nonJ variants. J has been related with a lower efficiency of electron transport chain (ETC), diminished ATP and ROS production. Thus, the difficult to compensate the mitochondrial energetic deficiency could explain the accumulation of J haplogroup in LHON and multiple sclerosis. Furthermore, the lower ROS production associated to J could also account for the accrual of this variant in elderly people consequent to a decreased oxidative damage.

摘要

这项研究调查了人类线粒体变异是否会影响最大耗氧量(VO₂max)。为此,我们招募了114名健康的西班牙男性受试者作为一个在饮食习惯和生活方式方面统一的群体,他们每周进行3 - 4次健身锻炼。一旦确定了线粒体DNA单倍群,我们发现J型单倍群的VO₂max低于非J型变异(P = 0.02)。J型单倍群与电子传递链(ETC)效率较低、ATP生成减少以及活性氧(ROS)生成减少有关。因此,难以补偿线粒体能量缺乏可能解释了J型单倍群在Leber遗传性视神经病变(LHON)和多发性硬化症中的积累。此外,与J型单倍群相关的较低ROS生成也可能解释了由于氧化损伤减少,该变异在老年人中的积累。

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