PAFの生合成並びに遊離に及ぼす食餌性脂質の効果

1.维生素E缺乏可刺激大鼠腹膜多形核白细胞（PMN）合成PAF。乙酰基转移酶的活性，转移的乙酰基部分的[3 H]乙酰辅酶A的lysoPAF从[3 H]PAF，较高的PMN匀浆从维生素E缺乏大鼠（2.28 - 0.07 nmol/min/mg蛋白）比那些从E补充大鼠（1.06 - 0.10 nmol/min/mg蛋白）。然而，有两组之间没有差异的乙酰水解酶的活性（4.26 0.71和4.26 0.06 nmol/min/mg蛋白质，分别），测定为[3 H]PAF降解为[3 H]lysoPAF。在体外添加-生育酚没有抑制活性增加的乙酰转移酶在维生素E缺乏的大鼠，表明维生素E补充大鼠的酶没有直接抑制-生育酚。两组的乙酰基转移酶对乙酰辅酶A显示出相似的Km值，但Vmax值不同（维生素E中为225 M和6.4 nmol/min/mg蛋白质）。 ...更多信息 缺乏维生素E的大鼠为216 nmol/min/mg蛋白质，补充维生素E的大鼠为3.6 nmol/min/mg蛋白质），表明维生素E缺乏时该酶未被激活，但数量增加. PAF的跨膜转运率明显高于lysoPAF。用PAF拮抗剂FR-900452预处理兔血小板后，PAF的跨膜转运率降至基础水平，与对照组lysoPAF的跨膜转运率相当。PAF预活化血小板可增强lysoPAF的转位。这些结果表明，加入少量lysoPAF激活PAF受体，可间接加速PAF穿过质膜脂双层体相的转运。在静息和活化血小板中，PAF lysoPAF通过质膜的易位被证明是这些化合物代谢转化为烷基酰基-GPC的速率限制。少

1. Vitamin E deficiency was found to stimulate FMLP-induced biosynthesis of PAF in polymorphonuclear leucocytes (PMN) from rat peritoneum. The activity of the acetyltransferase, which transfers the acetyl moiety of [3H] acetyl-CoA to lysoPAF to from [3H]PAF, higher in PMN homogenates from vitamin E-deficient rats (2.28 0.07 nmol/min/mg protein) than those from E-supplemented rats(1.06 0.10 nmol/min/mg protein). However, there was no difference between the two groups in the activity of the acetylhydrolase(4.26 0.71 and 4.26 0.06 nmol/min/mg protein, respectively), measured as degradation of [3H]PAF to [3H]lysoPAF. In vitro addition of -tocopherol did not inhibit the increased activity of acetyltransferase in vitamin E-deficient rats, indicating that the enzyme in vitamin E-supplemented rats was not directly inhibited by -tocopherol. The acethyltransferases of the two groups showed similar Km values for acetyl-CoA, but different Vmax values(225 M and 6.4 nmol/min/mg protein in vitamin E- … More deficient rats, and 216 m and 3.6 nmol/min/mg protein in vitamin E-supplemented rats), suggesting that the enzyme was not activated but increased in amount in vitamin E deficiency.2. The rate of translocation of PAF across rabbit platelet plasma membranes was significantly higher than that of lysoPAF. After pretreatment of rabbit platelets with the PAF antagonist FR-900452, the translocation rate of PAF was lowered to the basal rate, which was almost equal to that of lysoPAF across plasma membranes of control rabbit platelets. Converselv, the translocation of lysoPAF was augmented by pre-activation of the platelets by PAF. These results suggested that the translocation of PAF across the bulk phase of the lipid bilayer of plasma membranes can be accelerated indirectly by activation of PAF receptors by s small protion of added lysoPAF. In both resting and activated platelets, the translocations of PAF lysoPAF through the plasma membrance were shown to be rate-liniting for the metabolic conversions of these compounds to alkylacyl-GPC. Less