Inhibition of human platelet cyclooxygenase by alpha-tocopherol.

@article{Ali1980InhibitionOH,
  title={Inhibition of human platelet cyclooxygenase by alpha-tocopherol.},
  author={M. K. Ali and C G Gudbranson and Josh W. McDonald},
  journal={Prostaglandins and medicine},
  year={1980},
  volume={4 2},
  pages={
          79-85
        }
}
Influence of vitamin E on platelet function in humans.
  • M. Steiner
  • Medicine, Biology
    Journal of the American College of Nutrition
  • 1991
TLDR
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, and it is believed that dietary supplementation with this vitamin could play a role in the treatment of thromboembolic disease.
Effects of α-tocopherol (Vitamin E) on the Ultrastructure of Human Platelets In Vitro.
TLDR
The results show that the effects of tocopherol in washed platelet preparations are not comparable to those observed in plasma and that the platelet membrane must be regarded as a crucial target for vitamin E.
arachidonic acid metabolism, and plasma prostacyclin levels1
TLDR
A randomized, placebo-controlled double-blind trial was conducted on 20 adults to assess the effect of vitamin E on platelet function, arachidonic acid metabolism, and prostacycin generation, with no significant differences between the vitamin E and placebo groups.
Effects of alpha-tocopherol, its carboxylic acid chromane compound and two novel antioxidant isoflavanones on prostaglandin H synthase activity and autodeactivation
TLDR
These compounds serve as cosubstrates to which the oxidizing equivalents are transferred which arise during the hydroperoxidase reaction of the enzyme, and are suggested to protect the prostaglandin H synthase from rapid autodeactivation as revealed by repetitive application of AA in small doses.
Regulation of human leukocyte function by lipoxygenase products of arachidonic acid.
  • F. Valone
  • Biology
    Contemporary topics in immunobiology
  • 1984
TLDR
The lipoxygenase products of arachidonic acid are potent modulators of T-lymphocyte and PMN-function; these products may function both as extracellular mediators and as intracellular intermediates in cellular activation.
an ulceropermissive effect of vitamin E. To assess the effect of vitamin E on aspirin-induced gastric injury and mucosal prostan
TLDR
Aspirin markedly reduces mucosal prostanoid concentra tions in rats, without apparent effects on gastric injury, whereas vitamin E supplementation significantly reduced mucosal 6-keto prostaglandin Fia concentrations.
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References

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TLDR
The sharp rise in lipid peroxides normally associated with platelet aggregation was markedly reduced by alpha-tocopherol and also by acetylsalicylic acid, a known inhibitor of the platelet release reaction.
Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.
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Experiments with guinea-pig lung suggest that some of the therapeutic effects of sodium salicylate and aspirin-like drugs are due to inhibition of the synthesis of prostaglandins.
Effects of vitamin E on the aggregation and the lipid peroxidation of platelets exposed to hydrogen peroxide.
TLDR
The lipid peroxide formation associated with membrane disruption may be involved in the mechanism underlying the H2O2-induced platelet aggregation.
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TLDR
It is proposed that effects of sulfinpyrazone on platelet function may be due to inhibition of prostaglandin synthesis, which is a strong inhibitor of the release reaction under conditions of dilute collagent stimulation but is weak in the presence of stronger stimuli.
Aspirin selectively inhibits prostaglandin production in human platelets.
TLDR
Platelets in the blood of volunteers who have taken aspirin can no longer produce prostaglandins, and these platelets are removed from the body by the immune system.
ARACHIDONIC ACID PEROXIDATION, PROSTAGLANDIN SYNTHESIS AND PLATELET FUNCTION
TLDR
Results of the preliminary studies suggest that NBT and vitamin E can detect intermediates of lipid peroxidation, inhibit the conversion of arachidonic acid, prevent platelet aggregation and the release reaction without damaging the platelets morphologically or biochemically.
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