[Phosphoinositide breakdown and diacyl glycerin formation in human thrombocytes as affected by a lipopolysaccharide toxin].
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.
Viktorov
A V
AV
Dank
E Kh
EKh
Kuznetsov
V A
VA
Ter-Simonian
V G
VG
Iurkiv
V A
VA
D001427:Bacterial Toxins / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D002855:Chromatography, Thin Layer; D004075:Diglycerides / Q000096:biosynthesis* / Q000097:blood; D005989:Glycerides / Q000096:biosynthesis*; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology*; D010716:Phosphatidylinositols / Q000097:blood*; D010740:Phospholipases / Q000097:blood; D010974:Platelet Aggregation / Q000187:drug effects; D012486:Salmonella typhimurium; D013929:Thromboxane B2 / Q000096:biosynthesis
D001427:Bacterial Toxins; D004075:Diglycerides; D005989:Glycerides; D008070:Lipopolysaccharides; D010716:Phosphatidylinositols; D013929:Thromboxane B2; D010740:Phospholipases
Raspad fosfoinozitidov i obrazovanie diatsilglitserina v trombotsitakh cheloveka pod deĭstviem lipopolisakharidnogo toksina.