The events governing, intrinsic to and resulting from the immunologically induced secretion of the mediators of anaphylaxis from human and animal tissues are being studied. The relationship between cyclic GMP and enhanced release of mediators from human lung tissue was defined. The mechanism by which cyclic nucleotides modulate IgE-dependent mediator release reflects the state of assembly of microtubules. The release of mediators was associated with subsequent increases in cyclic AMP and cyclic GMP which were attributable to histamine interacting with H-1 and H-2 receptors. Stimulation of H-1 receptors results in cyclic GMP elevations and prostaglandin synthesis. Rat mast cells, human basophils and human lung mast cells release superoxide (O2) and superoxide dismutase (SOD) as a consequence of anaphylaxis. Both O2 and SOD were localized to the secretory granule. The RMC also generates O2 upon contacting schistosomula in the presence of immune serum. Human eosinophils, encountering C3b coated sepharose beads attach to the surface and secrete granule associated enzymes. The human platelet, like the eosinophil, contains aryl-sulfatase IIa and IIb. Partially purified aryl-sulfatase digests SRS-A. BIBLIOGRAPHIC REFERENCES: Kaliner, M.: The cholinergic nervous sytem and immediate hypersensivity. I. Eccrine sweat responses in allergic patients. J. Allergy Clin. Immunol. 58: 308-315, 1976. Kaliner, M., Blennerhassett, J. and Austen, K.F.: Bronchial asthma. In Meischer, P.A., and Muller-Eberhard, H.J. (Eds.): Textbook of Immunopathology. New York, Grune & Stratton, 1976, pp. 387-401.