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FMLP诱导的大鼠腹膜多形核白细胞(PMN)合成PAF。维生素E缺乏大鼠的中性粒细胞匀浆中，将[~3H]乙酰-辅酶A的乙酰基部分转移到溶解的PAF和形成[~3H]PAF的乙酰基转移酶的活性(2.28±0.07 nmol/min/mg蛋白)高于补充E的大鼠(1.06±0.10 nmol/min/mg蛋白)。而乙酰水解酶活性(分别为4.26±0.71和4.26±0.06 nmol/min/mg蛋白)与对照组比较差异无统计学意义(P>0.05)。在体外添加-生育酚不能抑制维生素E缺乏大鼠乙酰转移酶活性的升高，说明补充维生素E大鼠的乙酰基转移酶不是被-生育酚直接抑制的。两组乙酰基转移酶对乙酰辅酶A的Km值相似，但Vmax值不同(维生素E-…中的Vmax分别为225M和6.4nmol/分钟/mg蛋白补充维生素E的大鼠较缺乏维生素E的大鼠，其蛋白质含量分别为216m和3.6nmol/min/mg蛋白)，说明维生素E缺乏时，该酶没有被激活，而是增加了酶的量。PAF跨兔血小板膜的转移率明显高于溶血型PAF。用纤溶酶原激活剂拮抗剂FR-900452处理兔血小板后，纤溶酶原激活物的转移率降至基础水平，与对照兔血小板溶血性纤溶酶原激活物的跨膜转移率基本相同。PAF对血小板的预激活可增加溶质PAF的转位。这些结果表明，S通过激活PAF受体间接地加速了PAF跨膜脂双层整体相的转运。在静息和活化的血小板中，PAF溶体PAF通过质膜的移位对这些化合物向烷基酰基-GPC的代谢转化具有速率线性作用。较少

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