Graduate Center for Toxicology, University of Kentucky Medical Center, Lexington, KY 40536, USA.
Free Radic Biol Med. 2010 Jun 1;48(11):1535-9. doi: 10.1016/j.freeradbiomed.2010.02.035. Epub 2010 Mar 12.
Dietary coenzyme Q10 reduces spontaneous atherosclerosis in the apoE-deficient mouse model of experimental atherosclerosis. We have shown previously that exposure to sidestream cigarette smoke (SSCS) enhances atherosclerotic lesion formation in apoE-deficient mice. The aim of the present study was to determine if CoQ10 protected against SSCS-mediated atherosclerosis. Female apoE-deficient mice were fed a saturated fat-enriched diet (SFD) alone, or supplemented with 1% wt/wt coenzyme Q10 (SFD-Q10). Mice in each diet group were exposed to SSCS for 4hrs/day, 5days/week in a whole-body exposure chamber maintained at 35+/-4mg smoke particulates/m(3). Mice kept in filtered ambient air served as controls. Mice were euthanized after either 6 or 15weeks of SSCS exposure and following measurements were performed: i) lung 7-ethoxyresorufin-O-deethylase (EROD) activity; ii) plasma cholesterol and CoQ10 concentrations; iii) aortic intimal area covered by atherosclerotic lesions; and, iv) pathological characterization of lesions. Lung EROD activity increased in SSCS mice of both diet groups, confirming SSCS exposure. Plasma concentrations of CoQ10 in SFD-Q10-fed mice were increased markedly in comparison to SFD-fed mice. Plasma cholesterol concentrations and distributions of cholesterol in lipoprotein fractions were unaffected by SSCS exposure. Dietary supplementation with CoQ10 significantly reduced atherosclerotic lesions in control mice. As reported previously, exposure to SSCS increased the size of lesions in apoE-/- mice at both time points. However, dietary supplementation with CoQ10 had no effect on atherosclerotic lesions augmented by SSCS exposure. The results suggest a role of oxidative processes in smoke-augmented atherosclerosis that are different than those mitigated by CoQ10.
饮食辅酶 Q10 可减少实验性动脉粥样硬化 apoE 缺陷小鼠自发性动脉粥样硬化。我们之前已经表明，暴露于侧流香烟烟雾（SSCS）会增强 apoE 缺陷小鼠的动脉粥样硬化病变形成。本研究的目的是确定 CoQ10 是否可以预防 SSCS 介导的动脉粥样硬化。雌性 apoE 缺陷小鼠单独喂食富含饱和脂肪的饮食（SFD），或补充 1%wt/wt 辅酶 Q10（SFD-Q10）。每组饮食的小鼠在 35+/-4mg 烟雾颗粒/m(3)的全身暴露室中每天暴露于 SSCS 4 小时，每周 5 天。保持在过滤的环境空气中的小鼠作为对照。SSCS 暴露 6 或 15 周后，对小鼠进行安乐死，并进行以下测量：i）肺 7-乙氧基resorufin-O-脱乙基酶（EROD）活性；ii）血浆胆固醇和 CoQ10 浓度；iii）主动脉内膜面积覆盖的动脉粥样硬化病变；iv）病变的病理特征。两种饮食组的 SSCS 小鼠的肺 EROD 活性均增加，证实了 SSCS 的暴露。与 SFD 喂养的小鼠相比，SFD-Q10 喂养的小鼠的血浆 CoQ10 浓度明显增加。SSCS 暴露对血浆胆固醇浓度和脂蛋白中胆固醇的分布没有影响。膳食补充 CoQ10 可显著减少对照组小鼠的动脉粥样硬化病变。如前所述，暴露于 SSCS 会增加 apoE-/-小鼠在两个时间点的病变大小。然而，膳食补充 CoQ10 对 SSCS 暴露增强的动脉粥样硬化病变没有影响。结果表明，氧化过程在 SSCS 增强的动脉粥样硬化中起作用，与 CoQ10 减轻的作用不同。
