Influence of vitamin E on platelet function in humans

alpha-tocopherol, a natural antioxidant, has been found to inhibit platelet aggregation and release when tested in an in vitro system. This effect of vitamin E was thought to be due to a slight reduction of platelet cyclooxygenase activity and inhibition of lipid peroxide formation. Aggregation of platelets derived from individuals on a dietary supplementation of alpha-tocopherol ranging from 400 to 1200 IU/day showed no significant reduction. The discrepancy between the effectiveness of alpha-tocopherol in vitro and ex vivo is probably related to the levels of alpha-tocopherol attainable in platelets and plasma. Investigation of the effect of alpha-tocopherol on platelet adhesion showed a major inhibitory activity at doses of vitamin E as low as 200 IU/day. Measurements were performed in a laminar flow chamber at both high and low shear rates. Reduced platelet adherence to collagen, fibrinogen, and fibronectin could be documented. alpha-tocopherol-enriched platelets that adhered to adhesive surfaces failed to show the usual long thin pseudopodia but exhibited short, rounded, blunt projections. The reason for this shape change is still unclear, but we speculate that it may be causing the vitamin E-induced reduction of platelet adhesiveness. We believe that dietary supplementation with this vitamin could play a role in the treatment of thromboembolic disease, especially when given in conjunction with an inhibitor of platelet aggregation.