Elsbach P
J Lipid Res. 1967 Jul;8(4):359-65.
A comparison has been made between the conversion of (32)P-labeled lysophosphatidyl ethanolamine (LPE) and lysophosphatidyl choline (LPC) to their respective acylated and deacylated derivatives by homogenates of rabbit polymorphonuclear leukocytes and alveolar macrophages. Synthesis of PE by both homogenates and of PC by macrophage homogenates proceeded to about the same extent and is attributed to direct acylation of the lyso compounds. At higher LPC concentrations formation of PC by leukocytes is far greater than by macrophages. The mechanism of this enhanced synthesis of PC, which is brought out by higher substrate concentrations, is believed to be a transfer of the acyl group of one LPC molecule to another. Under optimal conditions macrophage homogenates deacylated LPE to a greater extent than LPC, while the reverse was true for leukocyte homogenates. Albumin inhibited deacylation of LPC and its conversion to PC by leukocytes, perhaps by binding the substrate (2 moles of LPC per mole of albumin). Other effects of albumin-stimulation of deacylation and acylation of LPE by macrophages, inhibition of deacylation and acylation of LPE by leukocytes-remain unexplained.
已对兔多形核白细胞和肺泡巨噬细胞匀浆将（32）P标记的溶血磷脂酰乙醇胺（LPE）和溶血磷脂酰胆碱（LPC）转化为各自的酰化和脱酰化衍生物的过程进行了比较。两种匀浆合成PE以及巨噬细胞匀浆合成PC的程度大致相同，这归因于溶血化合物的直接酰化。在较高的LPC浓度下，白细胞形成PC的量远大于巨噬细胞。较高底物浓度导致的PC合成增强的机制被认为是一个LPC分子的酰基转移到另一个LPC分子上。在最佳条件下，巨噬细胞匀浆使LPE脱酰的程度大于LPC，而白细胞匀浆则相反。白蛋白抑制白细胞将LPC脱酰及其转化为PC的过程，可能是通过结合底物（每摩尔白蛋白结合2摩尔LPC）。白蛋白对巨噬细胞脱酰和酰化LPE、对白细胞脱酰和酰化LPE的其他影响仍无法解释。
