Abstract
Although the effects of vitamin E on platelet function have been investigated in vivo and in vitro, vitamin E quinone, a natural metabolite of vitamin E, has been virtually overlooked. This oxidized form of vitamin E inhibits platelet aggregation and secretion induced by various aggregating agents more effectively than vitamin E by a magnitude of 5–10-fold. Vitamin E and vitamin E quinone do not alter platelet ultrastructure or cellular concentrations of serotonin and adenine nucleotides, including cAMP. Inhibition of aggregation by vitamin E quinone occurs in the absence of detectable reduction of vitamin E quinone or oxidation of vitamin E and is readily reversed by washing the platelet. Only vitamin E quinone prevents arachidonic acid release and slightly inhibits cyclooxygenase, whereas both agents partially prevent calcium release from a platelet subcellular organelle. Vitamin E quinone also inhibited synthesis of prostacyclin by endothelial cells with basal synthesis in the presence of external arachidonic acid being less affected than thrombin-stimulated PGI2 production. The greater potency of vitamin E quinone in suppressing platelet function compared to vitamin E suggests that this quinone metabolite may be the better antithrombotic agent and possibly responsible for in vivo effects previously attributed to vitamin E.
