Limited metabolic interaction of serine with ethanolamine and choline in the turnover of phosphatidylserine, phosphatidylethanolamine and plasmalogens in cultured glioma cells

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.