Cigarette smoke exposure and hypercholesterolemia increase mitochondrial damage in cardiovascular tissues
Cigarette smoke exposure and hypercholesterolemia increase mitochondrial damage in cardiovascular tissues
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DOI：
10.1161/hc0702.103977
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发表时间：
2002-02-19
期刊：
影响因子：
37.8
通讯作者：
Ballinger, SW
中科院分区：
文献类型：
--
作者：
Knight-Lozano, CA;Young, CG;Ballinger, SW
心血管疾病危险因素的一个共同特征是氧化应激增加。因为线粒体容易受到氧化应激介导的损伤，我们！假设危险因素（二手烟和高胆固醇血症）与心血管组织中线粒体损伤增加有关。方法和结果--对暴露于过滤空气或二手烟的年龄匹配的C57和apoE（-/-）小鼠的心血管组织中动脉粥样硬化病变形成、线粒体DNA损伤、蛋白质硝化和线粒体蛋白质的特异性活性进行定量。二手烟和高胆固醇血症都与线粒体DNA损伤和蛋白质硝化显著增加有关。烟草烟雾暴露也导致线粒体酶的比活性显着降低。二手烟和高胆固醇血症的组合导致动脉粥样硬化病变的形成增加，甚至更大的水平的线粒体damage. Conclusions，这些数据是一致的假设，心血管疾病的危险因素导致线粒体损伤和功能障碍。
Background-A shared feature among cardiovascular disease risk factors is increased oxidative stress. Because mitochondria are susceptible to damage mediated by oxidative stress; we! hypothesized that risk factors (secondhand smoke and hypercholesterolemia) are associated with increased mitochondrial damage in cardiovascular tissues.Methods and Results-Atherosclerotic lesion formation, mitochondrial DNA damage, protein nitration, and specific activities of mitochondrial proteins in cardiovascular tissues from age-matched C57 and apoE(-/-) mice exposed to filtered air or secondhand smoke were quantified. Both secondhand smoke and hypercholesterolemia were associated with significantly increased mitochondrial DNA damage and protein nitration. Tobacco smoke exposure also resulted in significantly decreased specific activities of mitochondrial enzymes. The combination of secondhand smoke and hypercholesterolemia resulted in increased atherosclerotic lesion formation and even greater levels of mitochondrial damage.Conclusions-These data are consistent with the hypothesis that cardiovascular disease risk factors cause mitochondrial damage and dysfunction.