Xu Z, Byers D M, Palmer F B, Spence M W, Cook H W
Atlantic Research Centre, Dalhousie University, Halifax, Canada.
Biochim Biophys Acta. 1993 Jun 12;1168(2):167-74. doi: 10.1016/0005-2760(93)90121-o.
Modulation of choline phosphoglyceride turnover has been investigated extensively but less is known about regulation of serine and ethanolamine phosphoglyceride synthesis and turnover. We investigated incorporation and interactions of [3H(G)]L-serine, [1,2-14C]ethanolamine and [methyl-3H]choline in cultured glioma cells. Exogenous serine did not compete with ethanolamine or choline incorporation and did not chase labeled headgroup from ethanolamine phosphoglycerides (PE); serine displaced headgroup of prelabeled phosphatidylserine (PtdSer) resulting in less labeled PtdSer for decarboxylation. In contrast, exogenous ethanolamine markedly chased labeled headgroup of non-plasmenylethanolamine phosphoglycerides (NP-PE) with less effect on plasmalogen (1-O-alk-1'-enyl-2-acyl-sn-glycero-3-phosphoethanolamine) whether headgroup was derived from [3H]serine or [14C]ethanolamine. Label in chase medium was mainly ethanolamine to 12 h; phosphoethanolamine was present with longer chase (12-48 h). Choline did not compete with serine incorporation and had little chase effect on PtdSer and PE. Choline and ethanolamine competitively interacted with preference for choline. These data suggest that (1) PtdSer synthesis in cultured glioma cells may involve more than headgroup exchange; (2) PE turnover with metabolite release to medium may involve both phospholipase D and phospholipase C; (3) acceleration of PE turnover by exogenous ethanolamine primarily involves NP-PE with lesser involvement of plasmalogen; and (4) in contrast to lack of interaction between serine and other headgroup precursors, choline and ethanolamine compete primarily at uptake.
胆碱磷酸甘油酯周转的调节已得到广泛研究，但关于丝氨酸和乙醇胺磷酸甘油酯合成与周转的调节了解较少。我们研究了[3H(G)]L-丝氨酸、[1,2-14C]乙醇胺和[甲基-3H]胆碱在培养的胶质瘤细胞中的掺入及相互作用。外源性丝氨酸不与乙醇胺或胆碱的掺入竞争，也不会从乙醇胺磷酸甘油酯（PE）中追出标记的头部基团；丝氨酸取代了预标记的磷脂酰丝氨酸（PtdSer）的头部基团，导致用于脱羧的标记PtdSer减少。相反，外源性乙醇胺显著追出非缩醛磷脂乙醇胺磷酸甘油酯（NP-PE）的标记头部基团，对缩醛磷脂（1-O-烯基-1'-烯基-2-酰基-sn-甘油-3-磷酸乙醇胺）的影响较小，无论头部基团是来自[3H]丝氨酸还是[14C]乙醇胺。在长达12小时的追踪培养基中标记物主要是乙醇胺；磷酸乙醇胺在更长时间的追踪（12 - 48小时）时出现。胆碱不与丝氨酸掺入竞争，对PtdSer和PE几乎没有追踪作用。胆碱和乙醇胺竞争性相互作用，更倾向于胆碱。这些数据表明：（1）培养的胶质瘤细胞中PtdSer的合成可能涉及不止头部基团交换；（2）PE周转及代谢产物释放到培养基中可能涉及磷脂酶D和磷脂酶C；（3）外源性乙醇胺加速PE周转主要涉及NP-PE，对缩醛磷脂的影响较小；（4）与丝氨酸和其他头部基团前体之间缺乏相互作用相反，胆碱和乙醇胺主要在摄取时竞争。
