Suzukawa M, Ishikawa T, Yoshida H, Nakamura H
1st Department of Internal Medicine, National Defense Medical College, Namiki Tokorozawa Saitama, Japan.
J Am Coll Nutr. 1995 Feb;14(1):46-52. doi: 10.1080/07315724.1995.10718472.
We have examined the effects of in-vivo supplementation with low-dose vitamin E on the susceptibility of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) to oxidative modification, and compared the oxidizability of HDL with that of LDL.
Normal humans (n = 8) ingested vitamin E (150 mg/day for 1 week, followed by 300 mg/day for 3 weeks) in divided doses with meals. The subjects did not use any medications or vitamins before being enrolled in this study. Fasting blood samples were drawn before and at the end of supplementation. LDL and HDL were separated by sequential ultracentrifugation and susceptability to copper-mediated oxidation was measured.
After vitamin E supplementation, vitamin E content of LDL increased 1.9-fold and that of HDL increased 1.8-fold. Lag time before initiation of LDL oxidation lengthened significantly (+20%, p < 0.01), and the propagation rate of LDL decreased significantly (-10%, p < 0.05). The lag time of HDL oxidation did not change significantly, but the propagation rate of HDL oxidation decreased significantly (-24%, p < 0.001). The lag time of HDL oxidation was shorter than that of LDL. HDL contained the same or higher concentrations of vitamin E relative to lipid mass as LDL, but contained lower concentration of CoQ10 relative to lipid mass and fewer molecules of vitamin E and beta-carotene per particle than LDL.
We conclude that in-vivo supplementation of low-dose vitamin E protects LDL against oxidative modification and decreases the propagation rate of HDL oxidation significantly. We suggest that supplementation with low-dose vitamin E would be beneficial for ameliorating atherosclerosis.
我们研究了体内补充低剂量维生素E对低密度脂蛋白(LDL)和高密度脂蛋白(HDL)氧化修饰敏感性的影响,并比较了HDL与LDL的氧化能力。
8名正常人随餐分剂量摄入维生素E(第1周150毫克/天,之后3周300毫克/天)。在参与本研究之前,受试者未使用任何药物或维生素。在补充前及补充结束时采集空腹血样。通过连续超速离心分离LDL和HDL,并测定其对铜介导氧化的敏感性。
补充维生素E后,LDL的维生素E含量增加了1.9倍,HDL的维生素E含量增加了1.8倍。LDL氧化开始前的延迟时间显著延长(+20%,p<0.01),LDL的氧化传播速率显著降低(-10%,p<0.05)。HDL氧化的延迟时间无显著变化,但HDL氧化的传播速率显著降低(-24%,p<0.001)。HDL氧化的延迟时间比LDL短。相对于脂质质量,HDL含有的维生素E浓度与LDL相同或更高,但相对于脂质质量,HDL含有的辅酶Q10浓度较低,且每个颗粒的维生素E和β-胡萝卜素分子数比LDL少。
我们得出结论,体内补充低剂量维生素E可保护LDL免受氧化修饰,并显著降低HDL氧化的传播速率。我们认为补充低剂量维生素E对改善动脉粥样硬化有益。