Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis
Effect of alcohol and tobacco smoke on mtDNA damage and atherogenesis
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DOI：
10.1016/j.freeradbiomed.2007.07.015
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发表时间：
2007-11-01
影响因子：
7.4
通讯作者：
Ballinger, Scott W.
中科院分区：
文献类型：
--
作者：
Cakir, Yavuz;Yang, Zhen;Ballinger, Scott W.
环境烟草烟雾（ETS）暴露和酒精（EtOH）消费通常同时发生，但其对心血管疾病发展的综合影响目前尚不清楚。ETS和EtOH暴露之间的共同特征是两者都增加线粒体内的氧化应激和功能障碍。本研究的假设是，与任一因素（ETS或EtOH）的单独作用相比，EtOH和ETS同时暴露将显著增加动脉粥样硬化形成和线粒体损伤。为了验证这一假设，apoE（-/-）小鼠暴露于EtOH和/或ETS单独或组合4周，并与过滤空气，非酒精对照进行比较。在血管组织中评估动脉粥样硬化病变形成（整个动脉油红O染色）、线粒体DNA（mtDNA）损伤和氧化应激。与过滤空气对照、酒精或单独暴露于ETS的动物相比，ETS和EtOH联合暴露对动脉粥样硬化形成、mIDNA损伤和氧化应激的影响最大。由于通常认为适量乙醇消费具有心脏保护作用，因此这些研究表明，应考虑常见心血管疾病风险因素（如烟草烟雾暴露或高胆固醇血症）对酒精心血管效应的潜在影响。(C)2007年爱思唯尔公司All rights reserved.
Environmental tobacco smoke (ETS) exposure and alcohol (EtOH) consumption often occur together, yet their combined effects on cardiovascular disease development are currently unclear. A shared feature between ETS and EtOH exposure is that both increase oxidative stress and dysfunction within mitochondria. The hypothesis of this study was that simultaneous EtOH and ETS exposure will significantly increase atherogenesis and mitochondrial damage compared to the individual effects of either factor (ETS or EtOH). To test this hypothesis, apoE(-/-) mice were exposed to EtOH and/or ETS singly or in combination for 4 weeks and compared to filtered air, nonalcohol controls. Atherosclerotic lesion formation (oil red O staining of whole aortas), mitochondrial DNA (mtDNA) damage, and oxidant stress were assessed in vascular tissues. Combined exposure to ETS and EtOH had the greatest impact on atherogenesis, mIDNA damage, and oxidant stress compared to filtered air controls, alcohol, or ETS-exposed animals alone. Because moderate EtOH consumption is commonly thought to be cardioprotective, these studies suggest that the potential influence of common cardiovascular disease risk factors, such as tobacco smoke exposure or hypercholesterolemia, on the cardiovascular effects of alcohol should be considered. (C) 2007 Elsevier Inc. All rights reserved.