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.
已对脂多糖毒素（LPS）与分离的洗涤过的人血血小板之间的相互作用进行了研究。发现LPS可诱导单磷酸和多磷酸肌醇迅速（1 - 2分钟）且显著（15 - 20%）分解，并形成大量二酰基甘油（约20%）。然而，LPS孵育仅使内源性14C - 花生四烯酸生成血栓素B2的生物合成增加约20%。磷脂酰胆碱和磷脂酰乙醇胺也分别被水解约8%和12%，推测是通过内源性磷脂酶A2的激活。此外，如使用硬脂酸多昔洛尔探针通过电子自旋共振光谱法所示，LPS导致血小板质膜的脂质流动性降低。LPS引起的所有这些变化均未诱导血小板聚集。得出的结论是，磷酸肌醇循环的增强并非血小板聚集可能的必要和充分条件。
