Tanaka K, Tokumaru S, Kojo S
Department of Food Science and Nutrition, Nara Women's University, Japan.
FEBS Lett. 1997 Aug 18;413(2):202-4. doi: 10.1016/s0014-5793(97)00917-4.
The role of oxidatively modified LDL in the pathogenesis of atherosclerosis has been well documented. These studies have focused on modifications of lipid and protein parts of LDL. Recently desialylated LDL has received attention in relation to atherosclerosis and coronary artery disease. We examined the possible involvement of radical reactions in desialylation of LDL. Human LDL was subjected to oxidative damage using Cu2+ ion. As the conjugated dienes monitored by absorption at 234 nm increased, the content of sialic acid decreased steadily. Both the elevation of conjugated diene and the decrease of sialic acid were inhibited by beta-mercaptoethanol, a typical radical scavenger. Besides, both butylated hydroxytoluene and a nitrogen atmosphere inhibited the decrease of sialic acid. These inhibition experiments suggested that sialic acid moieties in LDL were reactive toward radicals.
氧化修饰的低密度脂蛋白（LDL）在动脉粥样硬化发病机制中的作用已得到充分证明。这些研究集中在LDL的脂质和蛋白质部分的修饰上。最近，去唾液酸LDL在动脉粥样硬化和冠状动脉疾病方面受到了关注。我们研究了自由基反应在LDL去唾液酸化过程中可能的参与情况。使用铜离子（Cu2+）对人LDL进行氧化损伤。随着通过在234nm处的吸光度监测的共轭二烯增加，唾液酸的含量稳步下降。典型的自由基清除剂β-巯基乙醇抑制了共轭二烯的升高和唾液酸的减少。此外，丁基羟基甲苯和氮气气氛都抑制了唾液酸的减少。这些抑制实验表明LDL中的唾液酸部分对自由基具有反应性。
