Effects of copper-aspirin complex on washed platelet aggregation, thromboxane B(2) formation and 6-ketoprostaglandin F(1alpha) level were monitored by Born's and Terashita's methods, respectively. The influence of copper-aspirin complex on cytosolic free calcium was examined using the fluorescent indicator, Fura 2-AM. Copper-aspirin complex significantly inhibited arachidonic acid-induced aggregation in washed platelets. The IC(50) value was 9.6 micromol L(-1). Copper-aspirin complex significantly decreased arachidonic acid-induced thromboxane B(2) formation by 87.1% in washed platelets. Ten mg kg(-1) of copper-aspirin complex given intragastrically markedly increased the plasma level of 6-keto-prostaglandin F(1alpha). Aspirin, however, reduced both thromboxane B(2) formation and 6-keto-prostaglandin F(1alpha) level. In the presence of CaCl2 1 mmol L(-1), copper-aspirin complex (20, 40 and 80 micromol L(-1)) markedly lowered arachidonic acid-induced increase in platelet calcium from the resting level (270+/-36 nmol L(-1)) to 213+/-14, 170+/-20 and 135+/-17 nmol L(-1), respectively. In the presence of ethylene glycol-bis (beta-aminoethyl ether) N,N,N',N'-tetraacetic acid 1 mmol L(-1), copper-aspirin complex (20, 40 and 80 micromol l L(-1)) significantly suppressed the release of intracellular calcium induced by arachidonic acid from 127+/-23 nmol L-1 to 108+/-17, 93+/-12 and 70+/-13 nmol L(-1).