Patel R P, Boersma B J, Crawford J H, Hogg N, Kirk M, Kalyanaraman B, Parks D A, Barnes S, Darley-Usmar V
Department of Pathology, Molecular and Cellular Division, University of Alabama at Birmingham, Birmingham, AL 35294-0019, USA.
Free Radic Biol Med. 2001 Dec 15;31(12):1570-81. doi: 10.1016/s0891-5849(01)00737-7.
Oxidation of lipids has been implicated in the pathophysiology of atherosclerosis. It has been suggested that scavenging of lipid peroxyl radicals contribute to the antiatherosclerotic effects of naturally occurring compounds such as the isoflavones. This group of polyphenolics includes genistein and is present in relatively high concentrations in food products containing soy. Soy isoflavones are capable of inhibiting lipoprotein oxidation in vitro and suppressing formation of plasma lipid oxidation products in vivo. However, key aspects of the antioxidant mechanisms remain unknown. In this study the antioxidant effects of genistein and other soy isoflavones on lipid peroxidation initiated by mechanistically diverse oxidants was investigated. Although isoflavones inhibited lipid peroxidation stimulated by both metal-dependent and independent processes, the concentration required for these effects were relatively high compared to those found in vivo. Interestingly, however, isoflavones were not consumed and remained in the native state over the time during which inhibition of lipid peroxidation was observed. This was also the case under conditions where synergistic inhibition of LDL oxidation was observed with ascorbate. Furthermore, in an oxidation system driven solely by peroxyl radicals, isoflavones were found to be relatively poor peroxyl radical scavengers. Consistent with the apparent lack of reactivity with lipid-derived oxidants, isoflavones were also relatively resistant to oxidation mediated by the potent oxidant peroxynitrite. The potential antioxidant mechanisms of isoflavones are discussed in the context of possible reactivities of isoflavone-derived phenoxyl radicals.
脂质氧化与动脉粥样硬化的病理生理学有关。有人提出，清除脂质过氧自由基有助于天然存在的化合物（如异黄酮）发挥抗动脉粥样硬化作用。这类多酚类物质包括染料木黄酮，在含大豆的食品中含量相对较高。大豆异黄酮在体外能够抑制脂蛋白氧化，在体内能够抑制血浆脂质氧化产物的形成。然而，抗氧化机制的关键方面仍不清楚。在本研究中，研究了染料木黄酮和其他大豆异黄酮对由机制不同的氧化剂引发的脂质过氧化的抗氧化作用。尽管异黄酮抑制了由金属依赖性和非依赖性过程刺激的脂质过氧化，但与体内发现的浓度相比，产生这些作用所需的浓度相对较高。然而，有趣的是，在观察到脂质过氧化受到抑制的时间段内，异黄酮没有被消耗，而是保持在天然状态。在观察到与抗坏血酸协同抑制低密度脂蛋白氧化的条件下也是如此。此外，在仅由过氧自由基驱动的氧化系统中，发现异黄酮是相对较差的过氧自由基清除剂。与对脂质衍生氧化剂明显缺乏反应性一致，异黄酮对由强氧化剂过氧亚硝酸根介导的氧化也相对具有抗性。在异黄酮衍生的苯氧自由基可能的反应性背景下讨论了异黄酮的潜在抗氧化机制。
