Pieri C, Marra M, Gáspár R, Damjanovich S
Gerontological Research Department of I.N.R.C.A. Ancona, Italy.
Biochem Biophys Res Commun. 1996 May 15;222(2):256-60. doi: 10.1006/bbrc.1996.0731.
Protective effect of melatonin against Cu++ induced peroxidative modification of low density lipoprotein (LDL) was studied in vitro. Melatonin was used for this purpose because of its known scavenging capacity against hydroxyl and peroxyl radicals. It was demonstrated by the diene formation kinetic analysis that melatonin protected polyunsaturated fatty acids of LDL lipids against peroxidation. Lag time duration was prolonged, peak time was delayed, whereas rate of diene formation was decreased in melatonin treated LDL; however, parameters related to apolipoprotein (apo-B) showed that the protein was derivatized. Fluorescence, relative electrophoretic mobility, lysine residues analysis data, as well as the uptake by macrophages all showed properties similar to those of oxidised LDL. Present data suggest that by-products of melatonin oxidation might react with lysine residues of apo-B, transforming LDL in its atherogenic form.
在体外研究了褪黑素对铜离子诱导的低密度脂蛋白（LDL）过氧化修饰的保护作用。由于褪黑素已知具有清除羟基和过氧自由基的能力，因此用于此目的。通过二烯形成动力学分析表明，褪黑素可保护LDL脂质中的多不饱和脂肪酸免受过氧化。在褪黑素处理的LDL中，延迟时间延长，峰值时间延迟，而二烯形成速率降低；然而，与载脂蛋白（apo-B）相关的参数表明该蛋白质被衍生化。荧光、相对电泳迁移率、赖氨酸残基分析数据以及巨噬细胞摄取均显示出与氧化LDL相似的特性。目前的数据表明，褪黑素氧化的副产物可能与apo-B的赖氨酸残基反应，将LDL转化为其致动脉粥样硬化形式。
