Porkkala-Sarataho E K, Nyyssönen M K, Kaikkonen J E, Poulsen H E, Hayn E M, Salonen R M, Salonen J T
Research Institute of Public Health, University of Kuopio, Finland.
Am J Clin Nutr. 1998 Nov;68(5):1034-41. doi: 10.1093/ajcn/68.5.1034.
Supplementation with high doses of alpha-tocopherol has increased the oxidation resistance of LDL in many clinical trials. There have been only a few placebo-controlled trials in healthy persons of alpha-tocopherol doses usually contained in dietary supplements. We carried out a single-blind, placebo-controlled, randomized trial to examine the effect of 200 mg RRR-alpha-tocopheryl acetate/d on the oxidation resistance of atherogenic lipoproteins (VLDL+LDL including intermediate-density lipoproteins) in 40 smoking men. VLDL+LDL oxidation resistance was assessed as conjugated dienes after copper induction and hemin degradation after hydrogen peroxide induction. Also, the LDL total peroxyl-radical trapping antioxidant parameter (LDL TRAP) and plasma malondialdehyde were measured at baseline and after 2 mo of supplementation. Plasma RRR-alpha-tocopherol concentrations were measured at 2-h intervals for 12 h at baseline and after 2 mo of supplementation. Compared with placebo, 200-mg RRR-alpha-tocopheryl acetate supplementation elevated plasma and VLDL+LDL alpha-tocopherol concentrations, LDL TRAP, and oxidation resistance of VLDL+LDL. Plasma alpha-tocopherol increased by 88% (P < 0.0001), VLDL+LDL alpha-tocopherol increased by 90% (P < 0.0001), and LDL TRAP by 58% (P < 0.0001). The time to the start of oxidation (lag time) was prolonged by 34% when assessed with a copper-induced method and by 109% when assessed with a hemin + hydrogen peroxide-induced method; the time to maximal oxidation was prolonged by 21% (copper-induced method) in the vitamin E-supplemented group. Changes in plasma alpha-tocopherol, lipid-standardized alpha-tocopherol, and VLDL+LDL alpha-tocopherol correlated significantly with changes in LDL TRAP, lag time, and time to maximal oxidation. Differences in changes between groups in the area under the curve for plasma alpha-tocopherol were significant (P < 0.009). Our results suggest that 200 mg oral RRR-alpha-tocopheryl acetate/d had a clear effect on the in vitro oxidation of VLDL+LDL in smoking men.
在许多临床试验中，补充高剂量的α-生育酚可提高低密度脂蛋白（LDL）的抗氧化能力。针对膳食补充剂中常见的α-生育酚剂量，在健康人群中开展的安慰剂对照试验较少。我们进行了一项单盲、安慰剂对照的随机试验，以研究每日服用200毫克RRR-α-生育酚醋酸酯对40名吸烟男性中致动脉粥样硬化脂蛋白（极低密度脂蛋白+低密度脂蛋白，包括中间密度脂蛋白）抗氧化能力的影响。通过铜诱导后的共轭二烯以及过氧化氢诱导后的血红素降解来评估极低密度脂蛋白+低密度脂蛋白的抗氧化能力。此外，在基线期和补充2个月后，测量低密度脂蛋白总的过氧自由基捕获抗氧化参数（LDL TRAP）和血浆丙二醛。在基线期和补充2个月后，每隔2小时测量一次血浆RRR-α-生育酚浓度，持续12小时。与安慰剂相比，补充200毫克RRR-α-生育酚醋酸酯可提高血浆和极低密度脂蛋白+低密度脂蛋白中的α-生育酚浓度、LDL TRAP以及极低密度脂蛋白+低密度脂蛋白的抗氧化能力。血浆α-生育酚增加了88%（P<0.0001），极低密度脂蛋白+低密度脂蛋白α-生育酚增加了90%（P<0.0001），LDL TRAP增加了58%（P<0.0001）。用铜诱导法评估时，氧化开始时间（延迟时间）延长了34%，用过氧化氢+血红素诱导法评估时延长了109%；在维生素E补充组中，达到最大氧化的时间用铜诱导法评估时延长了21%。血浆α-生育酚、脂质标准化α-生育酚和极低密度脂蛋白+低密度脂蛋白α-生育酚的变化与LDL TRAP、延迟时间和达到最大氧化时间的变化显著相关。血浆α-生育酚曲线下面积的组间变化差异显著（P<0.009）。我们的结果表明，每日口服200毫克RRR-α-生育酚醋酸酯对吸烟男性极低密度脂蛋白+低密度脂蛋白的体外氧化有明显影响。
