Ascorbic acid enhances the formation of prostaglandin E1 in washed human platelets and prostacyclin in rat aortic rings.

  title={Ascorbic acid enhances the formation of prostaglandin E1 in washed human platelets and prostacyclin in rat aortic rings.},
  author={K. C. Srivastava},
  journal={Prostaglandins, leukotrienes, and medicine},
  volume={18 2},
  • K. C. Srivastava
  • Published 1 May 1985
  • Biology, Medicine
  • Prostaglandins, leukotrienes, and medicine
Inhibition of platelet activation using vitamins
The relationship between the vitamins that inhibit platelet aggregation and vascular diseases is examined and they may act synergistically or enhance the effects of endogenous anti-platelet compounds, such as prostacyclin or nitric oxide.
Effect of vitamin C and vitamin E on prostaglandin synthesis by fibroblasts and squamous carcinoma cells.
Essential Fatty Acids and Their Metabolites in the Pathobiology of Inflammation and Its Resolution
It is proposed that AA plays a crucial role in the pathobiology of ischemia/reperfusion injury, sepsis, COVID-19, and other critical illnesses, implying that its (AA) administration may be of significant benefit in the prevention and amelioration of these diseases.
Antioxidants and platelets.
It is suggested that antioxidants have an important role in the regulation of platelet function and clinical trials suggest that vitamin E reduced platelet aggregability.
Ascorbic acid and atherosclerotic cardiovascular disease.
The possible mechanisms by which ascorbic acid may affect the development of atherosclerosis and the onset of acute coronary events include effects on arterial wall integrity related to biosynthesis of collagen and GAGs, altered cholesterol metabolism mediated by vitamin C-dependent conversion of cholesterol to bile acids, and effects on triglyceride levels via modulation of lipoprotein lipase activity.


Vitamin C increases the formation of prostacyclin by aortic rings from various species and neutralizes the inhibitory effect of 15‐hydroperoxy‐arachidonic acid
1 Aortic rings from rats, rabbits and guinea‐pigs produce different amounts of 6‐oxo***‐prostaglandin F1α (6‐oxo‐PGF1α), the stable breakdown product of prostacyclin, i.e. 2760 ± 195, 160 ± 10 and 87
Influence of vitamin C on the metabolism of arachidonic acid and the development of aortic lesions during experimental atherosclerosis in rabbits.
Although there was a tendency to restore the prostacyclin output, vitamin C, in the amount administered, was unable to completely normalise the endothelial PGI2 production.
A mechanism for the hydroperoxide-mediated inactivation of prostacyclin synthetase.
Hydroxyl radical generation was demonstrated during heme-catalyzed decomposition of 15-hydroperoxy arachidonic acid. The hydroperoxide-mediated inactivation of prostacyclin synthetase seems to be
Aspects of the biosynthesis of prostaglandins.
Experiments did not confirm the view that prostaglandins could cure essential fatty acid deficient animals and the negative results of the experiments were attributed to the fact that PGE is rapidly metabolized when administered intravenously to rats.
Preparation of platelet suspensions from whole blood in buffer. Description of a method which gives a large platelet yield.
A simple method for preparation of platelet suspensions from whole blood in buffer is described. The platelets and a fraction of the erythrocytes are processed simultaneously, whereby the