The influence of vitamin E quinone on platelet structure, function, and
biochemistry
AC Cox, GH Rao, JM Gerrard and JG White
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.
Volume 55,
Issue 6,
pp. 907-914,
06/01/1980
Copyright © 1980 by The American Society of Hematology
