Bioenergetic and antioxidant properties of coenzyme Q10:: Recent developments
Bioenergetic and antioxidant properties of coenzyme Q10:: Recent developments
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DOI：
10.1007/s12033-007-0052-y
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发表时间：
2007-09-01
影响因子：
2.6
通讯作者：
Tiano, Luca
中科院分区：
文献类型：
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作者：
Littarru, Gian Paolo;Tiano, Luca
多年来，辅酶 Q（人类的 CoQ(10)）因其在线粒体生物能学中的关键作用而闻名。后来的研究证明了它存在于其他亚细胞部分和血浆中，并广泛研究了它的抗氧化作用。这两个功能构成了支持 CoQ(10) 临床应用的研究的基础。同样在线粒体内膜水平上，辅酶 Q 被认为是解偶联蛋白质功能的必需辅助因子和过渡孔的调节剂。此外，最近的数据表明，CoQ(10) 影响与人类细胞信号传导、代谢和运输有关的基因的表达，外源施用 CoQ(10) 的一些作用可能是由于这种特性。辅酶Q是唯一一种内源合成的脂溶性抗氧化剂。还原形式的 CoQH(2)（泛醇）可抑制蛋白质和 DNA 氧化，但其对脂质过氧化的影响得到了最深入的研究。泛醇抑制细胞膜脂质的过氧化以及循环中存在的脂蛋白脂质的过氧化。膳食补充 CoQ(10) 会导致循环脂蛋白中泛醇-10 的水平增加，并增加人类低密度脂蛋白对脂质过氧化起始的抵抗力。此外，CoQ(10) 具有直接的抗动脉粥样硬化作用，这已在高脂饮食喂养的载脂蛋白 E 缺陷小鼠中得到证实。在该模型中，补充药理学剂量的CoQ(10)能够降低动脉粥样硬化病变中脂质氢过氧化物的绝对浓度，并最小化整个主动脉中动脉粥样硬化病变的大小。这些保护作用是否仅归因于辅酶 Q 的抗氧化特性仍有待确定；最近的数据指出，CoQ(10) 可能对内皮功能产生直接影响。在稳定型中度 CHF 患者中，口服 CoQ(10) 补充剂可改善心肌收缩力和内皮功能障碍。我们实验室的最新数据显示，内皮结合的细胞外 SOD (ecSOD) 与血流依赖性内皮介导的扩张（通常用作血管功能生物标志物的功能参数）之间存在很强的相关性。该研究还强调补充 CoQ(10) 会显着影响内皮结合的 ecSOD 活性。此外，我们发现补充 CoQ(10) 后内皮结合 ecSOD 活性的增加与 FMD 的改善之间存在显着相关性。在 ecSOD 基础值较低的患者中，效果更为明显。最后，我们总结了我们实验室的研究结果，即 CoQ(10) 对精液完整性和精子细胞活力的影响。
For a number of years, coenzyme Q (CoQ(10) in humans) was known for its key role in mitochondrial bioenergetics; later studies demonstrated its presence in other subcellular fractions and in plasma, and extensively investigated its antioxidant role. These two functions constitute the basis on which research supporting the clinical use of CoQ(10) is founded. Also at the inner mitochondrial membrane level, coenzyme Q is recognized as an obligatory co-factor for the function of uncoupling proteins and a modulator of the transition pore. Furthermore, recent data reveal that CoQ(10) affects expression of genes involved in human cell signalling, metabolism, and transport and some of the effects of exogenously administered CoQ(10) may be due to this property. Coenzyme Q is the only lipid soluble antioxidant synthesized endogenously. In its reduced form, CoQH(2), ubiquinol, inhibits protein and DNA oxidation but it is the effect on lipid peroxidation that has been most deeply studied. Ubiquinol inhibits the peroxidation of cell membrane lipids and also that of lipoprotein lipids present in the circulation. Dietary supplementation with CoQ(10) results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoproteins to the initiation of lipid peroxidation. Moreover, CoQ(10) has a direct anti-atherogenic effect, which has been demonstrated in apolipoprotein E-deficient mice fed with a high-fat diet. In this model, supplementation with CoQ(10) at pharmacological doses was capable of decreasing the absolute concentration of lipid hydroperoxides in atherosclerotic lesions and of minimizing the size of atherosclerotic lesions in the whole aorta. Whether these protective effects are only due to the antioxidant properties of coenzyme Q remains to be established; recent data point out that CoQ(10) could have a direct effect on endothelial function. In patients with stable moderate CHF, oral CoQ(10) supplementation was shown to ameliorate cardiac contractility and endothelial dysfunction. Recent data from our laboratory showed a strong correlation between endothelium bound extra cellular SOD (ecSOD) and flow-dependent endothelial-mediated dilation, a functional parameter commonly used as a biomarker of vascular function. The study also highlighted that supplementation with CoQ(10) that significantly affects endothelium-bound ecSOD activity. Furthermore, we showed a significant correlation between increase in endothelial bound ecSOD activity and improvement in FMD after CoQ(10) supplementation. The effect was more pronounced in patients with low basal values of ecSOD. Finally, we summarize the findings, also from our laboratory, on the implications of CoQ(10) in seminal fluid integrity and sperm cell motility.