Fuller C J, May M A, Martin K J
Department of Nutrition & Foodservice Systems, The University of North Carolina at Greensboro, 27402-6170, USA.
J Am Coll Nutr. 2000 Jun;19(3):361-9. doi: 10.1080/07315724.2000.10718932.
The purpose of this study was to determine the effect of vitamin E and/or vitamin C supplementation on low-density lipoprotein (LDL) oxidizability and neutrophil (PMN) superoxide anion production in young smokers.
Thirty smokers with a <5 pack-year history were randomly assigned to take placebo; vitamin C (1 g/day); vitamin E (400 IU/day), or both vitamins in a double-blind fashion. Subjects took the supplements for 8 weeks. At weeks 0 and 8, blood was collected for isolation of LDL and PMN, and for antioxidant vitamin analysis. LDL was oxidized with a copper (Cu) catalyst, and oxidation was measured by formation of conjugated dienes over a 5-hour time course. Lag times and maximum oxidation rates were calculated from the time course data. PMN superoxide anion release was assessed by respiratory burst after stimulation with phorbol ester and opsonized zymosan, and their ability to oxidize autologous LDL following treatment with the above stimuli was measured with the conjugated diene assay.
Subjects who received vitamin E alone had a significant increase in the lag phase of Cu-catalyzed LDL oxidation (week 0, 118+/-31 min vs. week 8, 193+/-80 min, mean +/- SD, p < 0.05), whereas the vitamin C and placebo groups had no changes in LDL oxidation kinetics. The group receiving both vitamins E and C had a significant reduction in oxidation rate (week 0. 7.4+/-2.3 vs. week 8, 5.1+/-2.1, p < 0.05). There were no significant changes for any group in PMN superoxide anion production or PMN LDL oxidation after stimulation with either phorbol ester or opsonized zymosan. Plasma and LDL vitamin E concentrations were significantly increased in both groups that received vitamin E. The subjects who received vitamin C alone had no significant change in plasma vitamin C concentrations; however, when data were pooled from both groups who received vitamin C, the increases were significant.
Vitamin E supplementation of young smokers was effective in reducing Cu-catalyzed LDL oxidizability; however, vitamin E and/or C supplementation showed few significant effects on the more physiologically relevant PMN function. This casts doubt on the ability of antioxidant supplementation to reduce oxidative stress in smokers in vivo. Therefore, smoking cessation remains the only means by which young smokers can prevent premature coronary heart disease.
本研究旨在确定补充维生素E和/或维生素C对年轻吸烟者低密度脂蛋白（LDL）氧化能力及中性粒细胞（PMN）超氧阴离子生成的影响。
30名吸烟史<5包年的吸烟者被随机分配，以双盲方式服用安慰剂、维生素C（1克/天）、维生素E（400国际单位/天）或两种维生素。受试者服用补充剂8周。在第0周和第8周，采集血液以分离LDL和PMN，并进行抗氧化维生素分析。用铜（Cu）催化剂氧化LDL，并在5小时的时间进程中通过共轭二烯的形成来测量氧化。根据时间进程数据计算延迟时间和最大氧化速率。用佛波酯和调理酵母聚糖刺激后，通过呼吸爆发评估PMN超氧阴离子释放，并用共轭二烯测定法测量上述刺激处理后它们氧化自身LDL的能力。
单独接受维生素E的受试者，铜催化的LDL氧化延迟期显著增加（第0周，118±31分钟 vs. 第8周，193±80分钟，均值±标准差，p<0.05），而维生素C组和安慰剂组的LDL氧化动力学无变化。同时接受维生素E和C的组氧化速率显著降低（第0周，7.4±2.3 vs. 第8周，5.1±2.1，p<0.05）。用佛波酯或调理酵母聚糖刺激后，任何组的PMN超氧阴离子生成或PMN LDL氧化均无显著变化。接受维生素E的两组血浆和LDL维生素E浓度均显著增加。单独接受维生素C的受试者血浆维生素C浓度无显著变化；然而，当汇总接受维生素C的两组数据时，增加是显著的。
补充维生素E对年轻吸烟者降低铜催化的LDL氧化能力有效；然而，补充维生素E和/或C对更具生理相关性的PMN功能几乎没有显著影响。这使人怀疑补充抗氧化剂在体内降低吸烟者氧化应激的能力。因此，戒烟仍然是年轻吸烟者预防过早冠心病的唯一方法。
