Is tartrazine-induced asthma related to inhibition of prostaglandin biosynthesis?
Since it has been suggested that aspirin-induced asthma is due to inhibition of prostaglandin (PG) biosynthesis, the present investigation was undertaken to determine whether tartrazine would display a similar profile. Use was made of the exquisite sensitivity of blood platelets, both in humans and in rats, to aggregating substances generated from arachidonic acid during PG biosynthesis and of the ability of aspirin to inhibit aggregation and generation of those substances. Failure to affect aggregation by arachidonic acid as well as the accompanying formation of thromboxane A2, demonstrates that neither tartrazine nor its metabolite sulfanilic acid inhibit platelet PG synthesis. It seems unlikely that tartrazine-induced asthma results from inhibition of PG biosynthesis.
D001241:Aspirin / Q000009:adverse effects / Q000494:pharmacology; D001249:Asthma / Q000139:chemically induced / Q000378:metabolism*; D001391:Azo Compounds / Q000494:pharmacology*; D001792:Blood Platelets / Q000502:physiology; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D013425:Sulfanilic Acids / Q000494:pharmacology; D013645:Tartrazine / Q000009:adverse effects / Q000494:pharmacology*; D013928:Thromboxane A2 / Q000096:biosynthesis
D001391:Azo Compounds; D011453:Prostaglandins; D013425:Sulfanilic Acids; D013928:Thromboxane A2; D013645:Tartrazine; D001241:Aspirin