Dowty B J, Rodriguez de Turco E, Hagar A, Spitzer J A
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Circ Shock. 1992 Apr;36(4):307-11.
The opsonized zymosan-stimulated turnover of 32P-labeled phospholipids was examined in alveolar macrophages from rats 3 hr after intravenous administration of saline or a nonlethal dose of endotoxin. Stimulation resulted in increased incorporation of [32P]PO4 into phosphatidic acid and phosphatidylinositol. Also a decreased [32P]phosphatidylcholine and an increased [32P]lysophosphatidylcholine labeling were observed, suggesting an increased activity of phosphatidylcholine-specific phospholipase A2. Endotoxin attenuated these changes in 32P-labeled phospholipids, demonstrating the ability of a nonlethal dose of endotoxin to perturb phospholipid-dependent signal transduction mechanisms in cells isolated from a compartment other than the one in which endotoxin was administered.
在静脉注射生理盐水或非致死剂量内毒素3小时后，检测大鼠肺泡巨噬细胞中调理酵母聚糖刺激的32P标记磷脂的周转情况。刺激导致[32P]PO4掺入磷脂酸和磷脂酰肌醇增加。还观察到[32P]磷脂酰胆碱减少和[32P]溶血磷脂酰胆碱标记增加，提示磷脂酰胆碱特异性磷脂酶A2活性增加。内毒素减弱了32P标记磷脂的这些变化，表明非致死剂量的内毒素能够扰乱从不同于内毒素给药部位的隔室分离出的细胞中依赖磷脂的信号转导机制。
