Upon stimulation of surface membranes of non-exitable cells, such as polymorphonuclear leukocytes and platelets, a number of metabolic changes are induced via a transmembrane control mechanism in which mobilization of Ca2+ in the biological membrane may play a critical role (1,3,9,11,14, 18, 24). Thus, the search for the triggering mechanism for intracellular metabolic activation has focussed on the determination of compounds by which the mobilization of cytoplasmic Ca2+ is controlled (6,8,10,16, 19, 22, 23). It is known that perturbation of surface membranes of these cells increases arachidonic acid metabolism and the turnover of phospholipids within the membrane/lipid bilayer, followed by release of their metabolites (4, 13, 15). Several investigators have suggested that certain oxidized metabolites (endoperoxides) of polyunsaturated long-chain fatty acids, such as arachidonic acid and its metabolites, increase membrane permeability for Ca2+ this effect is abolished by reducing the metabolites with SnCl2 (19, 20). Although the putative ionophoretic action of these metabolites for Ca2+ has received considerable attention, the biophysical functions of arachidonic acid and its metabolites have not been fully elucidated. Liposomes entrapped with Quin II, an indicator of Ca2+, have been used as a highly sensitive assay system for Ca2+ ionophoresis; formation of Quin II-Ca2+ complex markedly increases the fluorescence intensity at 490 nm (21). The present work demonstrates that several unsaturated long-chain fatty acids including arachidonic acid increase the translocation of Ca2+ across liposomal membrane.Ca2+ binds to Quin II in a stoichiometric ratio of one to one, and the fluorescence intensity is proportional to the logarithm of the concentration of Ca2+-Quin II complex. When CaCl2 (1 mM) was added to the incubation medium, the fluorescence Abbreviations used: DPPC, dipalmitoyl phosphatidyl choline; DCP, dicetyl phosphate.