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Can mitochondrial dysfunction be a predictive factor for oxidative stress in patients with obstructive sleep apnea?

机译:线粒体功能障碍能否成为阻塞性睡眠呼吸暂停患者氧化应激的预测因素?

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摘要

Mitochondrial dysfunction reflects a lifelong cumulative burden of cellular damage, and a decrease in mitochondrial DNA (mtDNA) copy number is associated with oxidative stress and chronic inflammation. The goal of this study was to assess whether mitochondrial dysfunction and a decrease in mtDNA copy number are common features of patients with obstructive sleep apnea syndrome (OSA). We compared mtDNA copy number between 20 healthy volunteers and 20 patients with OSA and investigated whether a significant attenuation of mtDNA copy number was observed in genomic DNA isolated from whole blood of OSA patients. Our observations lead to the hypothesis that mtDNA copy number is lower in whole blood DNA of OSA subjects and might be related to OSA severity, reflecting excessive oxidative stress in patients with OSA.
机译:线粒体功能障碍反映了终生的细胞损伤累积负担,线粒体DNA(mtDNA)拷贝数的减少与氧化应激和慢性炎症有关。这项研究的目的是评估线粒体功能障碍和mtDNA拷贝数减少是否是阻塞性睡眠呼吸暂停综合症(OSA)患者的共同特征。我们比较了20名健康志愿者和20例OSA患者的mtDNA拷贝数,并调查了在从OSA患者全血分离的基因组DNA中是否观察到mtDNA拷贝数的显着降低。我们的观察结果提出了这样的假设:在OSA受试者的全血DNA中mtDNA拷贝数较低,并且可能与OSA严重程度有关,这反映了OSA患者的过度氧化应激。

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