Further studies on the effects of flavine adenine dinucleotide on the platelet functions.
Flavine adenine dinucleotide (FAD) may inhibit not only the aggregation but also ATP release of platelets in vitro. FAD did not inhibit the synthesis of thromboxane from 1-14C-arachidonic acid by platelets. FAD was found to be hydrolyzed to FMN and AMP by a plasma enzyme, the activity of which in normal adults being estimated as 32.6 +/- 9.1 m microM/ml plasma/min and AMP, thus produced, and/or FAD might compete for the receptor sites on the platelet surface. This could be the mechanism of the inhibitory effect of FAD upon the platelet functions. The intravenous drip infusion of FAD in a dose of 0.2 mg/kg within 30 min was followed by no marked decrease of platelet aggregation, probably because the plasma concentration of FAD and/or AMP did not reach the levels high enough to suppress the platelet functions.
D000255:Adenosine Triphosphate / Q000097:blood; D000328:Adult; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000097:blood; D001792:Blood Platelets / Q000201:enzymology / Q000502:physiology*; D005182:Flavin-Adenine Dinucleotide / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D006868:Hydrolysis; D010974:Platelet Aggregation
D001095:Arachidonic Acids; D005182:Flavin-Adenine Dinucleotide; D016718:Arachidonic Acid; D000255:Adenosine Triphosphate