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 linoleic and oleic acids caused a poisoning epidemic, known as Toxic Oil Syndrome, in Spain in 1981. Toxic Oil Syndrome affected mainly the lungs and the immune system of exposed individuals. Linoleic and oleic acids, and linoleic and oleic anilides increased the production of reactive oxygen metabolites in human polymorphonuclear leukocytes. Both cis-fatty acids inhibited a chemotactic peptide-, fMLP-induced production of reactive oxygen metabolites without affecting fMLP-induced elevation of intracellular calcium levels. Linoleic acid anilide slightly amplified fMLP-induced respiratory burst, whereas oleic acid anilide was without an effect. However, both fatty acid anilides decreased fMLP-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 (DiC8)-induced production of reactive oxygen metabolites. Thus, both cis-fatty acids and their anilides inhibited agonist-stimulated production of reactive oxygen metabolites; this is most likely due to interactions with cell signalling events. These results suggest that both linoleic and oleic acids and their anilides may inhibit immunological responses of leukocytes.