Viana M, Barbas C, Bonet B, Bonet M V, Castro M, Fraile M V, Herrera E
Centro de Ciencias Experimentales y Técnicas, Universidad de San Pablo, CEU, Boadilla del Monte, Madrid, Spain.
Atherosclerosis. 1996 Jun;123(1-2):83-91. doi: 10.1016/0021-9150(95)05763-3.
Flavonoids are phenolic compounds of vegetable origin with antioxidant effects. The present study aimed to determine their properties as LDL antioxidants. LDL were incubated with increasing concentrations of flavonoids (0-16 micrograms/ml) and LDL oxidation was started by adding CuCl2 (2 microM) to the media. When flavonoids were present in the media, vitamin E consumption, the lag phase of conjugated diene formation, LDL electrophoretic mobility in agarose gels and the appearance of thiobarbituric acid reacting substances (TBARS) were delayed in a concentration-dependent manner. To determine whether flavonoids could terminate LDL oxidation once initiated, two sets of experiments were performed. In the first, LDL oxidation was initiated as described above. At 2 or 4 h of incubation, flavonoids were added (4 micrograms/ml) and their effect compared to samples where butylated hydroxytoluene or EDTA were added. At 5 h, in the LDL samples where flavonoids were added, the electrophoretic mobility and TBARS production were the same as those present in LDL samples incubated for the whole period in the absence of flavonoids. However, when either butylate hydroxytoluene or EDTA was added, as would be expected, the LDL oxidation process was completely arrested as shown by a reduction in the appearance of TBARS and a lower LDL electrophoretic mobility. In the second experiment, LDL oxidation was initiated as described above and at 0, 10 and 20 min, flavonoids were added (4 micrograms/ml). When vitamin E was still present in the LDL solution, the flavonoids were able to both increase the lag phase in the formation of conjugated dienes and to delay the consumption of vitamin E. The present results show that in vitro, flavonoids prevent LDL oxidation in a concentration-dependent manner, delaying the consumption of vitamin E, but they cannot terminate or delay LDL oxidation once vitamin E in LDL is consumed.
类黄酮是具有抗氧化作用的植物源性酚类化合物。本研究旨在确定它们作为低密度脂蛋白（LDL）抗氧化剂的特性。将LDL与浓度不断增加的类黄酮（0 - 16微克/毫升）一起孵育，并通过向培养基中添加CuCl2（2微摩尔）启动LDL氧化。当培养基中存在类黄酮时，维生素E的消耗、共轭二烯形成的延迟期、LDL在琼脂糖凝胶中的电泳迁移率以及硫代巴比妥酸反应物质（TBARS）的出现均以浓度依赖的方式延迟。为了确定类黄酮一旦启动是否能终止LDL氧化，进行了两组实验。在第一组实验中，如上述启动LDL氧化。在孵育2或4小时时，添加类黄酮（4微克/毫升），并将其效果与添加丁基化羟基甲苯或乙二胺四乙酸（EDTA）的样品进行比较。在5小时时，在添加类黄酮的LDL样品中，电泳迁移率和TBARS产生与在无类黄酮的情况下孵育整个时期的LDL样品中的情况相同。然而，当添加丁基化羟基甲苯或EDTA时，正如预期的那样，LDL氧化过程完全停止，这表现为TBARS出现减少和LDL电泳迁移率降低。在第二个实验中，如上述启动LDL氧化，并在0、10和20分钟时添加类黄酮（4微克/毫升）。当LDL溶液中仍存在维生素E时，类黄酮既能增加共轭二烯形成的延迟期，又能延迟维生素E的消耗。目前的结果表明，在体外，类黄酮以浓度依赖的方式预防LDL氧化，延迟维生素E的消耗，但一旦LDL中的维生素E被消耗，它们就不能终止或延迟LDL氧化。
