Delattre J, Bonnefont-Rousselot D, Khalil A, Lepage S, Gardes-Albert M, Ferradini C
Laboratoire de Biochimie, Hôpital de la Salpêtrière, Paris.
Bull Acad Natl Med. 1993 Oct;177(7):1251-60; discussion 1260-2.
The involvement of low density lipoprotein (LDL) peroxidation in atherogenesis is now admitted. The oxidation of high density lipoproteins (HDL) could contribute to the atherogenic process, by limiting their capacity to accept cholesterol from cell membranes. In this work, we studied the human HDL peroxidation initiated by OH. or OH./O2.- free radicals generated by gamma radiolysis. This method allows a quantitative and selective production of free radicals, and the resulting oxidation is less drastic than the chemical one. HDL oxidation was followed, as a function of the radiation dose, by the disappearance of endogenous vitamin E, the formation of thiobarbituric acid-reactive substances (TBARS) and the fluorescence at 440 nm. Human HDL turned out to be oxidizable by hydroxyl free radicals and oxygen potentiated this effect. The oxidative modification of HDL, leading to a rigidification of the HDL envelop, could contribute to reduce the ability of HDL to stimulate efflux of cholesterol from tissues.
目前已公认低密度脂蛋白(LDL)过氧化参与动脉粥样硬化的形成。高密度脂蛋白(HDL)的氧化可能会通过限制其从细胞膜接受胆固醇的能力而促进动脉粥样硬化进程。在这项研究中,我们研究了由γ射线分解产生的OH·或OH·/O₂⁻自由基引发的人HDL过氧化。该方法可定量且选择性地产生自由基,并且由此产生的氧化作用比化学氧化作用的剧烈程度要小。通过内源性维生素E的消失、硫代巴比妥酸反应性物质(TBARS)的形成以及440nm处的荧光,跟踪HDL氧化随辐射剂量的变化情况。结果表明,人HDL可被羟基自由基氧化,并且氧气会增强这种作用。HDL的氧化修饰导致HDL包膜变硬,这可能会降低HDL刺激组织中胆固醇流出的能力。