Vitamin E inhibits the release of calcium from a platelet fraction in vitro.
Vitamin E, an inhibitor of platelet aggregation, was evaluated for its effects on platelet intracellular calcium flux. These studies used a platelet membrane fraction containing membranes of the dense tubular system which actively sequesters calcium in the presence of ATP and magnesium. After these membrane vesicles have accumulated calcium, the cation can be released by addition of the calcium ionophore A23187. Vitamin E had no effect on uptake of calcium by the membrane vesicles, but showed a concentration dependent inhibition of the release of calcium induced by A23187. In similar or slightly higher concentrations than inhibited calcium release, vitamin E also inhibited platelet aggregation, internal contraction and secretion, but had no effect on prostaglandin and thromboxane synthesis and potentiated phospholipase A2 activity. It is suggested that vitamin E acts to inhibit platelet internal contraction and secretion by preventing efflux of calcium from the dense tubular system. The potentiation of phospholiplase A2 by vitamin E could be explained by a localized increase of calcium at the site of the phospholipase A2 on the inner side of the dense tubular system membrane proximal to the vitamin E block.
D001095:Arachidonic Acids / Q000097:blood; D001711:Biotransformation; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000097:blood*; D006801:Humans; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism; D010741:Phospholipases A / Q000097:blood; D054467:Phospholipases A2; D010974:Platelet Aggregation / Q000187:drug effects; D014810:Vitamin E / Q000494:pharmacology*
D001095:Arachidonic Acids; D014810:Vitamin E; D000001:Calcimycin; D010741:Phospholipases A; D054467:Phospholipases A2; D002118:Calcium