Tartrazine and the prostaglandin system.
The effect of tartrazine on prostaglandin production was evaluated in several in vitro systems in order to elucidate the interrelationship between aspirin-sensitive asthma and tartrazine. Unlike the nonsteroidal anti-inflammatory drugs, tartrazine did not inhibit cyclooxygenase activity in sheep seminal vesicles, guinea pig lung microsomes, and human platelets. Tartrazine had no effect on the activation of acyl hydrolase, which is the rate-limiting step in prostaglandin production. The major metabolite of tartrazine, sulfanilic acid, also had no inhibitory effect on the sheep seminal vesicle cyclooxygenase. In view of these findings, if there is a cross-sensitivity between tartrazine and aspirin in aspirin-sensitive asthmatics, it is unlikely to be on the basis of prostaglandin inhibition.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D001391:Azo Compounds / Q000009:adverse effects*; D006168:Guinea Pigs; D006801:Humans; D008297:Male; D010105:Oxygenases / Q000037:antagonists & inhibitors; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D012756:Sheep; D013425:Sulfanilic Acids / Q000378:metabolism; D013645:Tartrazine / Q000009:adverse effects*; D013931:Thromboxanes / Q000037:antagonists & inhibitors
D001095:Arachidonic Acids; D001391:Azo Compounds; D011453:Prostaglandins; D013425:Sulfanilic Acids; D013931:Thromboxanes; D010105:Oxygenases; D013645:Tartrazine