The role of arachidonate lipoxygenase in the release of SRS-A from guinea-pig chopped lung.
The immunological release of SRS-A was investigated in guinea-pig chopped lung. A number of unsaturated fatty acids, all of which are substrates for arachidonate lipoxygenase were found to potentiate the release of SRS-A. This potentiation was enhanced by indomethacin, a cyclo-oxygenase inhibitor, and completely reversed by nordihydroguaiaretic acid (NDGA) and eicosatetraynoic acid (ETA) which inhibit lipoxygenase. This suggests that some aspect of arachidonate lipoxygenase action stimulates release of SRS-A and that release of SRS-A is increased by redirection of arachidonic acid (AA) metabolism via the lipoxygenase pathway (Hamberg, 1976). However, although exogenous 14C-AA increased SRS-A output it was not incorporated into SRS-A.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism*; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology; D006168:Guinea Pigs; D006636:Histamine Release / Q000187:drug effects; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008084:Lipoxygenase / Q000502:physiology*; D008168:Lung / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D008297:Male; D011453:Prostaglandins / Q000378:metabolism; D013189:SRS-A / Q000378:metabolism*
D001095:Arachidonic Acids; D005231:Fatty Acids, Unsaturated; D011453:Prostaglandins; D013189:SRS-A; D008084:Lipoxygenase; D007213:Indomethacin