Dietary vitamin E supplementation inhibits thrombin‐induced platelet aggregation, but not monocyte adhesiveness, in patients with hypercholesterolaemia

Abstract

Several recent studies have indicated the possible beneficial effects of antioxidants, specifically vitamin E, in primary and secondary coronary prevention. These studies suggest that a diet enriched in vitamin E is insufficient to have a significant protective effect, whereas supplements, in excess of 200 international units (IU) per day, are efficacious in preventing coronary disease in both men and women. The mechanisms by which vitamin E may exert its protection are uncertain, but, vitamin E is lipophilic and has been shown to inhibit the oxidative modification of low density lipoprotein (LDL), a process thought to be of crucial importance in atherogenesis. We have also previously shown that alpha-tocopherol (the biologically most potent isomer of vitamin E) has important direct effects on vascular endothelial and smooth muscle cells. In the present study we have investigated the effects of oral supplements of vitamin E (400 IU per day) on platelet and mononuclear cell function in patients with hypercholesterolaemia. We found that although vitamin E supplementation had no significant effect on mononuclear cell adhesion ex vivo, it had a significant effect on the thrombin-induced platelet aggregation (P < 0.01; ANOVA): 6 weeks after starting the vitamin E supplements, the mean EC50 for thrombin-induced aggregation increased 132% (P < 0.05; paired t-test) compared to treatment with placebo. The effects of vitamin E on platelet function may, in part, explain its anti-atherogenic properties.

Optimal nutrition: vitamin E

“…Supplementation of hypercholesterolaemic patients with vitamin E (267 mg α-TE/d for 6 weeks) resulted in a significant inhibition of thrombin-induced aggregation (Williams et al 1997). After 6 weeks supplementation, the mean concentration producing 50 % maximum effect for thrombin-induced aggregation increased 132 % (P < 0·05).…”

“…However, some authors (Williams et al 1997) are of the opinion that the effects of vitamin E on platelet function could explain in part its anti-atherogenic properties.…”

Nutrition, Supplements, and Vitamins in Platelet Function and Bleeding

“…As shown in Table 4, among the 7 trials [122][123][124][125][126][127][128] in patients at risk of cardiovascular disease, 5 were performed in patients with diabetes mellitus. In these 5 trials, [122][123][124][125][126] the daily amount of vitamin E ranged from 100 to 600 IU, and follow-up lasted from 2 to 10 weeks.…”

“…125 In the remaining 2 studies performed in smokers or patients with dyslipidemia, inhibition of or no change in platelet function, respectively, was reported. 127,128 Globally considered, trials exploring the effect of vitamin E on platelet function inconsistently showed an inhibitory property in healthy subjects. The positive data obtained in diabetic patients are of some interest but are flawed by several methodological reasons, including nonsystematic analysis of oxidative stress and antioxidant status, open design, and small sample size.…”

Vitamin E 80th Anniversary: A Double Life, Not Only Fighting Radicals

“…These events are relevant to the onset of in ammation as well as in the early stages of atherogenesis. ®-Tocopherol inhibits aggregation of human platelets by a PKCdependent mechanism both in vitro and in vivo (53,(67)(68)(69). Also°-tocopherol decreases more potently than ®-tocopherol, suggesting that an antioxidant mechanism is not applicable given the lesser antioxidant activity of the latter relative to ®-tocopherol (68).…”