Viktorov A V, Dank E Kh, Kuznetsov V A, Ter-Simonian V G, Iurkiv V A
Biull Eksp Biol Med. 1988 Mar;105(3):291-4.
The interaction of lipopolysaccharide toxin (LPS) with isolated washed human blood platelets has been studied. LPS was found to induce the rapid (1-2 min) and marked (15-20%) breakdown of mono- and polyphosphoinositides and formation of significant amounts of diacylglycerols (ca. 20%). However TxB2 biosynthesis from endogenous 14C-arachidonic acid was stimulated by LPS incubation only by ca. 20%. Phosphatidylcholine and phosphatidylethanolamine were also hydrolysed by ca. 8 and 12%, respectively, presumably via the activation of endogenous phospholipase A2. Besides, LPS caused the decreasing of the lipid fluidity of a platelet plasma membrane as was shown by ESR spectroscopy using doxylstearic acid probes. All these changes by LPS induce no aggregation of platelets. It is concluded that an enhancement of a phosphoinositide cycle is not a possibly necessary and sufficient condition for a platelet aggregation.