Phosphatidylethanolamine biosynthesis in isolated hamster heart.

The pathways leading to the formation of phosphatidylethanolamine in isolated hamster hearts were investigated. The contributions of the CDP-ethanolamine and the base exchange pathways were studied by perfusion with [3H]ethanolamine. The radioactivity of ethanolamine in the heart reached a maximum at 5 min of perfusion and remained constant throughout the perfusion period. Maximum labeling of phosphoethanolamine occurred at 25 min of perfusion and labeling of CDP-ethanolamine did not reach a maximum over the 30-min-perfusion period. Incorporation of radioactivity into phosphatidylethanolamine was marked by a lag during the first 15 min of perfusion, after which a linear increase was observed. This initial lag suggests the minor contribution of the base exchange pathway, as compared with the CDP-ethanolamine pathway. The CDP-ethanolamine pathway was estimated to contribute 290 nmol x min-1 x g heart-1 to total phosphatidylethanolamine formation in hamster heart. Phosphatidylethanolamine formation via decarboxylation of phosphatidylserine was studied by perfusion of hamster hearts with labeled serine. The contribution of this pathway was estimated to be 9.0 nmol x min-1 x g heart-1. Hence, it was concluded that phosphatidylethanolamine was synthesized by all three known pathways and the CDP-ethanolamine pathway was the major pathway for phosphatidylethanolamine biosynthesis in the mammalian heart. The low activities of phosphatidylserine decarboxylase and base exchange enzyme measured in vitro probably reflect the minor contribution of these two pathways to phosphatidylethanolamine biosynthesis.