Kapiotis Stylianos, Hermann Marcela, Exner Markus, Sturm Brigitte N, Scheiber-Mojdehkar Barbara, Goldenberg Hans, Kopp Stefan, Chiba Peter, Gmeiner Bernhard M K
Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Austria.
Free Radic Res. 2005 Nov;39(11):1225-31. doi: 10.1080/10715760500306968.
Al(3+) stimulates Fe(2+) induced lipid oxidation in liposomal and cellular systems. Low-density lipoprotein (LDL) oxidation may render the particle atherogenic. As elevated levels of Al(3+) and increased lipid oxidation of LDL are found in sera of hemodialysis patients, we investigated the influence of Al(3+) on LDL oxidation.
Using different LDL modifying systems (Fe(2+), Cu(2+), free radical generating compounds, human endothelial cells, hemin/H(2)O(2) and HOCl), the influence of Al(3+) on LDL lipid and apoprotein alteration was investigated by altered electrophoretic mobility, lipid hydroperoxide-, conjugated diene- and TBARS formation.
Al(3+) could stimulate the oxidizability of LDL by Fe(2+), but not in the other systems tested. Al(3+) and Fe(2+) were found to bind to LDL and Al(3+)could compete with Fe(2+) binding to the lipoprotein. Fluorescence polarization data indicated that Al(3+) does not affect the phospholipid compartment of LDL.
The results indicate that increased LDL oxidation by Fe(2+) in presence of Al(3+) might be due to blockage of Fe(2+) binding sites on LDL making more free Fe(2+) available for lipid oxidation.
铝离子（Al(3+)）在脂质体和细胞系统中可刺激亚铁离子（Fe(2+)）诱导的脂质氧化。低密度脂蛋白（LDL）氧化可能会使该颗粒具有致动脉粥样硬化性。由于在血液透析患者的血清中发现铝离子水平升高且LDL的脂质氧化增加，我们研究了铝离子对LDL氧化的影响。
使用不同的LDL修饰系统（Fe(2+)、Cu(2+)、自由基生成化合物、人内皮细胞、血红素/H₂O₂和次氯酸），通过改变的电泳迁移率、脂质氢过氧化物、共轭二烯和硫代巴比妥酸反应物（TBARS）的形成来研究铝离子对LDL脂质和载脂蛋白改变的影响。
铝离子可刺激Fe(2+)诱导的LDL氧化能力，但在其他测试系统中则不然。发现铝离子和Fe(2+)可与LDL结合，并且铝离子可与Fe(2+)竞争结合脂蛋白。荧光偏振数据表明铝离子不影响LDL的磷脂部分。
结果表明，在铝离子存在的情况下，Fe(2+)导致的LDL氧化增加可能是由于LDL上Fe(2+)结合位点被阻断，从而使更多游离的Fe(2+)可用于脂质氧化。
