Fuller C J, Grundy S M, Norkus E P, Jialal I
Department of Clinical Nutrition, University of Texas-Southwestern Medical Center, Dallas, USA.
Atherosclerosis. 1996 Jan 26;119(2):139-50. doi: 10.1016/0021-9150(95)05659-9.
The oxidative modification of low density lipoprotein (LDL) may play a role in the pathogenesis of atherosclerosis. Furthermore, evidence of oxidized LDL (ox-LDL) has been found in vivo. Supplementation of some animal models with antioxidants has been shown to retard the formation of aortic atherosclerosis. Ascorbate (vitamin C) is a highly potent aqueous-phase antioxidant in plasma, which has been shown in vitro to retard LDL oxidation. Cigarette smokers have reduced concentrations of ascorbate in their plasma, and their LDL may be more prone to oxidation. Hence, the objective of the present study was to examine the effect of ascorbate depletion and supplementation on the propensity of LDL to oxidize in smokers in a 6-week study. Nineteen healthy smokers followed a low ascorbate diet (< or = 30 mg/day) for 2 weeks, then were randomly assigned to receive placebo or 1000 mg ascorbate per day for 4 weeks. Blood was taken at 0 and 4 weeks of supplementation for study of LDL oxidative susceptibility. LDL was oxidized with 5 mumol/l copper. The ascorbate-supplemented group had significant increases in plasma ascorbate. The placebo group showed no change in the time course of LDL oxidation between 0 and 4 weeks. However, the ascorbate-supplemented group has a significant reduction in LDL oxidative susceptibility as measured by thiobarbituric acid-reactive substances (TBARS) and the formation of conjugated dienes. The ascorbate-supplemented group demonstrated significantly increased lag phase and decreased oxidation rate at 4 weeks compared to 0 weeks. No changes were found in the placebo group. The ascorbate-supplemented group showed no biochemical signs consistent with increased body iron stores. Supplementation of otherwise healthy smokers for 4 weeks with 1000 mg ascorbate per day resulted in increased plasma ascorbate and reduced LDL oxidative susceptibility.
低密度脂蛋白(LDL)的氧化修饰可能在动脉粥样硬化的发病机制中起作用。此外,体内已发现氧化型LDL(ox-LDL)的证据。在一些动物模型中补充抗氧化剂已显示可延缓主动脉粥样硬化的形成。抗坏血酸(维生素C)是血浆中一种高效的水相抗氧化剂,体外实验已表明它可延缓LDL氧化。吸烟者血浆中抗坏血酸浓度降低,其LDL可能更易氧化。因此,本研究的目的是在一项为期6周的研究中,检测抗坏血酸缺乏和补充对吸烟者LDL氧化倾向的影响。19名健康吸烟者遵循低抗坏血酸饮食(≤30毫克/天)2周,然后随机分配接受安慰剂或每天1000毫克抗坏血酸,持续4周。在补充的第0周和第4周采血,用于研究LDL的氧化易感性。用5微摩尔/升铜氧化LDL。补充抗坏血酸组的血浆抗坏血酸显著增加。安慰剂组在0至4周期间LDL氧化的时间进程无变化。然而,通过硫代巴比妥酸反应性物质(TBARS)和共轭二烯的形成来衡量,补充抗坏血酸组的LDL氧化易感性显著降低。与0周相比,补充抗坏血酸组在4周时的滞后期显著延长,氧化速率降低。安慰剂组未发现变化。补充抗坏血酸组未出现与体内铁储存增加一致的生化迹象。对原本健康的吸烟者每天补充1000毫克抗坏血酸4周,可导致血浆抗坏血酸增加,LDL氧化易感性降低。