The celluar interaction of ascorbic acid with histamine, cyclic nucleotides and prostaglandins in the immediate hypersensitivity reaction.
The role of ascorbic acid is reviewed in relation to the mechanism of release of chemical mediators in the immediate hypersensitivity reaction. In the initiation, and second, stages of the reaction, the property of ascorbic acid to chelate with calcium appears to play an importnat role in the ultimate release of the mediators. Furthermore, ascorbic acid may also control release of histamine and prostaglandins of the E and F types through its action on cyclic nucleotides and phosphodiesterase. In allergic inflammatory disease, leucocyte and tissue ascorbic acid levels are reduced. This may be due to the increased utilisation by cells involved in the antigen-antibody reaction. The suggestion that the balance between cyclic nucleotides is the main controlling mechanism for the release of chemical mediators during the reaction is inadequate to account for the essential role of other agents including ascorbic acid in the mechanism.
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism* / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism*; D006636:Histamine Release; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000378:metabolism*; D007962:Leukocytes / Q000378:metabolism; D010726:Phosphodiesterase Inhibitors / Q000378:metabolism; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000037:antagonists & inhibitors
D010726:Phosphodiesterase Inhibitors; D011458:Prostaglandins E; D011460:Prostaglandins F; D000242:Cyclic AMP; D006152:Cyclic GMP; D001205:Ascorbic Acid; D002118:Calcium