INHIBITORY EFFECT OF LYSOPHOSPHATIDYLCHOLINE AND PHOSPHOLIPASE A(2) -TREATED LOW-DENSITY LIPOPROTEINS ON RECEPTOR-DEPENDENT REGULATION OF [CA2+](I) IN PLATELETS

Treatment of LDL with phospholipase A(2) from bee venom resulted in fo rmation of lipid-protein particles (pl-LDL) with increased content of lysophosphatidylcholine (LPC). At the same time, composition of other lipids and protein structure were unaffected, Both pl-LDL and LPC abol ished PAF-, ADP- and thrombin-induced Ca2+ elevation in platelets and platelet aggregation, while LDL had no effect on hormone-stimulated in crease in the intracellular Ca2+ content ([Ca2+](i)), The effect persi sted in Ca2+-free medium, indicating that pl-LDL and LPC also abolish Ca2+ mobilisation from intracellular stores, Neither LPC nor pl-LDL ch anged platelet Ca2+ levels and inhibited platelet aggregation induced by phorbolmyristate acetate, a PKC activator, and thapsigargin, a spec ific inhibitor of the endoplasmic reticulum Ca2+ ATPase, The inhibitor y effect depended on LPC concentration, incubation time and the struct ure of LPC: lysophosphatidylethanolamine and phosphatidylcholine produ ced no inhibitory effect. The half-maximum-effective concentrations we re the same for LPC and pl-LDL (2-4 mu M), The results obtained indica te that LPC and pl-LDL inhibit the receptor-dependent increase in Ca2, It can be suggested that the effect of LPC is mediated by redistribu tion of the plasma membrane integral proteins, which leads to disinteg ration of the intracellular signalling systems.