Kögl C, Schneider W, Elstner E F
Technische Universität München, Lehrstuhl für Phytophathologie, Weihenstephan, Germany.
Biochem Pharmacol. 1994 Jun 15;47(12):2201-6. doi: 10.1016/0006-2952(94)90256-9.
Low density lipoprotein (LDL) in the presence of magnesium-pyridoxal-5'-phosphate-glutamate (MPPG), pyridoxal-5'-phosphate (PP), alpha-tocopherol, probucol or trolox is more resistant against copper-induced oxidation as control-LDL in vitro. The efficiency of the drugs is: probucol > MPPG > trolox > alpha-tocopherol > PP. LDL oxidation is determined by its increasing negative surface charge, fragmentation of apolipoprotein B-100 and changes of the fatty acid content of LDL. The protection of the drugs depends on their concentration and incubation time. Different experiments point to the fact that copper-induced oxidation of LDL in vitro starts with the binding of copper at the apolipoprotein B-100, resulting in an increasing negative surface charge and fragmentation of the apolipoprotein B-100. Afterwards a decrease of LDL-bound linoleic acid (18:2) is measurable.
在体外,与对照低密度脂蛋白(LDL)相比,低密度脂蛋白在存在镁-吡哆醛-5'-磷酸-谷氨酸(MPPG)、吡哆醛-5'-磷酸(PP)、α-生育酚、普罗布考或生育三烯酚时,对铜诱导的氧化更具抗性。这些药物的效果依次为:普罗布考>MPPG>生育三烯酚>α-生育酚>PP。LDL氧化通过其表面负电荷增加、载脂蛋白B-100片段化以及LDL脂肪酸含量变化来确定。药物的保护作用取决于其浓度和孵育时间。不同实验表明,体外铜诱导的LDL氧化始于铜与载脂蛋白B-100结合,导致表面负电荷增加和载脂蛋白B-100片段化。随后可检测到LDL结合的亚油酸(18:2)减少。