Jürgens G, Fell A, Ledinski G, Chen Q, Paltauf F
Institut für Medizinische Biochemie, Karl-Franzens Universität Graz, Austria.
Chem Phys Lipids. 1995 Aug 1;77(1):25-31. doi: 10.1016/0009-3084(95)02451-n.
Low density lipoprotein (LDL) isolated from human serum of different donors was enriched with plasmalogens and their diacyl analogs in order to investigate a possible effect of these phospholipids on the rate of lipid peroxidation in this lipoprotein. LDL was incubated with either vesicles of choline plasmalogen or phosphatidylcholine in presence of lipoprotein- deficient serum, or with liposomes of ethanolamine plasmalogen or phosphatidylethanolamine together with the non-specific phospholipid transfer protein isolated from beef liver. After re-isolation of LDL by ultracentrifugation, a dose-dependent incorporation of the exogenous phospholipids was obtained. Enrichment of LDL with choline plasmalogen resulted in a delay of the copper-catalyzed oxidation of LDL from five different donors. LDL from two donors was also enriched with diacylglycerophosphocholine which led to a delay of oxidation, but the protective effect was smaller than with choline plasmalogen. Enrichment of LDL from two additional donors with ethanolamine plasmalogen resulted in the strongest protection against oxidation, whereas, diacylglycerophospho-ethanolamine had little effect. The delay of the copper-catalyzed LDL oxidation may be due to a direct antioxidative action of the plasmalogens, which are partially degraded during the lag phase of oxidation, or to an indirect effect caused by alteration of the LDL surface in the presence of an excess of glycerophospholipids.
从不同供体的人血清中分离出的低密度脂蛋白（LDL）用缩醛磷脂及其二酰基类似物进行富集，以研究这些磷脂对该脂蛋白脂质过氧化速率的可能影响。在缺乏脂蛋白的血清存在下，将LDL与胆碱缩醛磷脂或磷脂酰胆碱的囊泡一起孵育，或者将LDL与乙醇胺缩醛磷脂或磷脂酰乙醇胺的脂质体以及从牛肝中分离出的非特异性磷脂转移蛋白一起孵育。通过超速离心重新分离LDL后，获得了外源磷脂的剂量依赖性掺入。用胆碱缩醛磷脂富集LDL导致来自五个不同供体的LDL的铜催化氧化延迟。来自两个供体的LDL也用二酰基甘油磷酸胆碱进行了富集，这导致氧化延迟，但保护作用小于胆碱缩醛磷脂。用乙醇胺缩醛磷脂对另外两个供体的LDL进行富集产生了最强的抗氧化保护作用，而二酰基甘油磷酸乙醇胺几乎没有作用。铜催化的LDL氧化延迟可能是由于缩醛磷脂的直接抗氧化作用，缩醛磷脂在氧化的延迟期会部分降解，或者是由于在存在过量甘油磷脂的情况下LDL表面改变所引起的间接作用。
