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线粒体功能障碍能否作为阻塞性睡眠呼吸暂停患者氧化应激的预测因素?

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

作者信息

Kim Yoo-Suk, Kwak Jin Wook, Lee Kyu Eun, Cho Hyun Sang, Lim Su Jin, Kim Kyung Soo, Yang Hoon Shik, Kim Hyun Jik

机构信息

1 Department of Otolaryngology, Ajou University School of Medicine , Suwon, Korea.

出版信息

Antioxid Redox Signal. 2014 Sep 20;21(9):1285-8. doi: 10.1089/ars.2014.5955. Epub 2014 Jul 21.

DOI:10.1089/ars.2014.5955
PMID:24926527
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4158965/
Abstract

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.

摘要

线粒体功能障碍反映了细胞损伤的终身累积负担,线粒体DNA(mtDNA)拷贝数的减少与氧化应激和慢性炎症相关。本研究的目的是评估线粒体功能障碍和mtDNA拷贝数减少是否为阻塞性睡眠呼吸暂停综合征(OSA)患者的常见特征。我们比较了20名健康志愿者和20名OSA患者的mtDNA拷贝数,并研究从OSA患者全血中分离的基因组DNA中是否观察到mtDNA拷贝数的显著衰减。我们的观察结果得出一个假设,即OSA受试者全血DNA中的mtDNA拷贝数较低,且可能与OSA严重程度相关,反映了OSA患者存在过度氧化应激。

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