【摘要】 在人肺癌表皮细胞株A 5 49中检测到佛波酯诱导的丁醇化鞘脂分子的产生。用 [3H] 丝氨酸标记细胞 ,其放射性在磷脂酰胆碱、磷脂酰丝氨酸、磷脂酰乙醇胺极性头部的分布很容易被检测到 ,而在磷脂酸及其直接代谢衍生物中并不存在 ,提示这种磷脂酶D的酶解产物来源于鞘脂分子的水解 ,而不同于以甘油磷脂为底物的磷脂酶D的酶解产物。蛋白激酶C的抑制剂或通过佛波酯长时间处理下调细胞内蛋白激酶C水平 ,可抑制佛波酯诱导的丁醇化鞘脂分子的产生 ,表明导致这种磷脂酶D的活化需要蛋白激酶C的参与更多还原

【Abstract】 It is demonstrated here that phorbol 12 myristate 13 acetate (PMA) induced the formation of a butanolated sphingolipids in A 549 cells. In cells labeled with [ 3H] serine, the distribution of the radioactivity was easily found in phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylethanolamine (PE), but not in phosphatidic acid (PA) and its immediate metabolic derivatives, suggesting that the newly detected PLD products were derived from sphingolipids and were different from the conventional product of PLD. Protein kinase C (PKC) inhibitors or PKC down regulation by prolonged PMA treatment inhibited the PMA induced generation of this butanolated sphingolipid, indicating that PKC activation was required in this process.更多还原