INTERACTIONS OF CIS-FATTY ACIDS AND THEIR ANILIDES WITH FORMYL-METHIONYL-LEUCYL-PHENYLALANINE, PHORBOL-MYRISTATE ACETATE AND DIOCTANOYL-S,N-GLYCEROL IN HUMAN-LEUKOCYTES

Aniline-denaturated rape-seed food oils that contained anilides of lin oleic and oleic acids caused a poisoning epidemic, known as Toxic Oil Syndrome, in Spain in 1981. Toxic Oil Syndrome affected mainly the lun gs and the immune system of exposed individuals. Linoleic and oleic ac ids, and linoleic and oleic acid anilides increased the production of reactive oxygen metabolites in human polymorphonuclear leukocytes. Bot h cis-fatty acids inhibited a chemotactic peptide-, fMLP-induced produ ction of reactive oxygen metabolites without affecting fMLP-induced el evation of intracellular calcium levels. Linoleic acid anilide slightl y amplified fMLP-induced respiratory burst, whereas oleic acid anilide was without an effect. However, both fatty acid anilides decreased fM LP-induced elevation of levels of free intracellular calcium. Moreover , both cis-fatty acids and their anilides inhibited phorbol myristate acetate (PMA)- and dioctanoyl-s,n-glycerol (DiC(8))-induced production of reactive oxygen metabolites. Thus, both cis-fatty acids and their anilides inhibited agonist-stimulated production of reactive oxygen me tabolites; this is most likely due to interactions with cell signallin g events. These results suggest that both linoleic and oleic acids and their anilides may inhibit immunological responses of leukocytes.