Tyurin V A, Carta G, Tyurina Y Y, Banni S, Day B W, Corongiu F P, Kagan V E
Department of Environmental & Occupational Health, University of Pittsburgh, Pennsylvania 15238, USA.
Lipids. 1997 Feb;32(2):131-42. doi: 10.1007/s11745-997-0017-0.
Recent studies provide extensive evidence for the importance of carotenoids in protecting against oxidative stress associated with a number of diseases. In particular, reactions of carotenoids with phenoxyl radicals generated by peroxidase-catalyzed one-electron metabolism of phenolic compounds may represent an important antioxidant function of carotenoids. To further our understanding of the antioxidant mechanisms of carotenoids, we used in the present work two different phenolic compounds, phenol and a polar homologue of vitamin E (2,2,5,7,8-pentamethyl-6-hydroxychromane, PMC), as representatives of two different types of phenols to study reactions of their respective phenoxyl radicals with carotenoids in cells and in model systems. We found that phenoxyl radicals of PMC did not oxidize beta-carotene in either HL-60 cells or in model systems with horseradish peroxidase (HRP)/H2O2. In contrast, the phenoxyl radicals generated from phenol (by native myeloperoxidase in HL-60 cells or HRP/H2O2 in model systems) effectively oxidized beta-carotene and other carotenoids (canthaxanthin, lutein, lycopene). One-electron reduction of the phenoxyl radical by ascorbate (assayed by electron spin resonance-detectable formation of semidehydroascorbyl radicals) prevented HRP/H2O2-induced oxidation of beta-carotene. PMC, but not phenol, protected beta-carotene against oxidation induced by a lipid-soluble azo-initiator of peroxyl radicals. No adducts of peroxidase/phenol/H2O2-induced beta-carotene oxidation intermediates with phenol were detected by high-performance liquid chromatography-mass spectrometry analysis of the reaction mixture. Since carotenoids are essential constituents of the antioxidant defenses in cells and biological fluids, their depletion through the reaction with phenoxyl radicals formed from endogenous, nutritional and environmental phenolics, as well as phenolic drugs, may be an important factor in the development of oxidative stress.
近期研究提供了大量证据，证明类胡萝卜素在预防与多种疾病相关的氧化应激方面具有重要作用。特别是，类胡萝卜素与酚类化合物过氧化物酶催化的单电子代谢产生的苯氧自由基的反应，可能代表了类胡萝卜素的一种重要抗氧化功能。为了进一步了解类胡萝卜素的抗氧化机制，我们在本研究中使用了两种不同的酚类化合物，即苯酚和维生素E的极性同系物（2,2,5,7,8-五甲基-6-羟基色满，PMC），作为两种不同类型酚的代表，来研究它们各自的苯氧自由基与细胞和模型系统中的类胡萝卜素的反应。我们发现，PMC的苯氧自由基在HL-60细胞或辣根过氧化物酶（HRP）/H2O2模型系统中均不会氧化β-胡萝卜素。相比之下，由苯酚产生的苯氧自由基（在HL-60细胞中由天然髓过氧化物酶产生，或在模型系统中由HRP/H2O2产生）能有效氧化β-胡萝卜素和其他类胡萝卜素（角黄素、叶黄素、番茄红素）。抗坏血酸对苯氧自由基的单电子还原作用（通过电子自旋共振检测到半脱氢抗坏血酸自由基的形成来测定）可防止HRP/H2O2诱导的β-胡萝卜素氧化。PMC能保护β-胡萝卜素免受过氧自由基的脂溶性偶氮引发剂诱导的氧化，而苯酚则不能。通过对反应混合物进行高效液相色谱-质谱分析，未检测到过氧化物酶/苯酚/H2O2诱导的β-胡萝卜素氧化中间体与苯酚的加合物。由于类胡萝卜素是细胞和生物体液中抗氧化防御的重要组成部分，它们与内源性、营养性和环境性酚类以及酚类药物形成的苯氧自由基反应而消耗，可能是氧化应激发生发展的一个重要因素。
