In both animals and humans, vitamin E deficiency is associated with platelet hyperaggregability. In six E-deficient children, thrombocytosis was associated with marked hyperaggregability of their platelets to ADP, epinephrine, and collagen. Platelet malonyldialdehyde (MDA) formation was used as an indicator of prostaglandin formation, and was found to be increased during the E deficiency state. Following E repletion, both platelet aggregation and platelet MDA formation returned to normal. The addition of vitamin E to platelets in vitro has been associated with inhibition of platelet release, aggregation, and MDA formation.
Extending these in vitro observations further, six normal controls were given 1600 units of vitamin E orally daily for 2 weeks to elevate their plasma E levels and the E content of their platelets in vivo. Concomitant with the elevation in their plasma E levels, there was an inhibitory effect of 12–20% on platelet MDA formation following E ingestion. These studies suggest that E deficiency increases the in vivo synthesis of platelet endoperoxides and prostaglandins, and that E excess has the opposite effect, i.e., inhibition of the endoperox-ide intermediates of prostaglandin synthesis.
Several phenolic antioxidants such as α-tocopherol or vitamin E, butylated hydroxytoluene, and propylgallate inhibit lipid peroxidation. These compounds inhibit the oxidation reactions catalyzed by cyclo-oxygenase(2,1) and lipoxidase(3,4) to varying degrees. In 1966, Nugteren et al.(1) demonstrated that high concentrations of the antioxidants, propylgallate and vitamin E, inhibited prostaglandin biosynthesis in a paniculate fraction of the sheep vesicular gland. These antioxidants inhibit the in vitro peroxidation of arachidonic acid, which is catalyzed by sheep vesicular gland dioxygenase.