246 V. OXIDATION AND METABOLISM OF PHOSPHOLIPIDS 



group of phospholipids originally referred to as"cephalins," and now iden- 

 tified more specifically as "phosphatidylethanolamine." 



b. Sources of Ethanolamine in the Animal Body. Several compounds 

 which can be readily synthesized physiologically in the animal body may 

 serve as mother substances for ethanolamine. These include glycine/^ 

 and possibly serineJ^ Presumably glycine is first converted to serine, and 

 this compound becomes ethanolamine when decarboxylation has been ef- 

 fected. There is ample proof that glycine and serine are interconvertible. 

 Shemin" was the first to prove that glycine can originate from serine, while 

 a number of workers^*"" proved the reverse reaction, namely the glycine 

 ->• serine reaction. According to Sakami,^^ formate condenses WTth glycine 

 to form serine; the formate carbon becomes the 13 carbon of the newly- 

 synthesized amino acid. This was demonstrated experimentally by using 

 C^^-formate and C^^-1-glycine as the reactants, as follows: 



NHzCHa-CsOOH 4- HChOOH > HOCHHsCHNHa-CisOOH 



The Combination of Glycine and Formate to Form Serine'* 



Siekevitz and Greenberg''^ reported that one molecule of glycine may con- 

 tribute the a-carbon to form formate, which then condenses with a second 

 molecule of glycine to yield serine. 



The conversion of serine to ethanolamine was first suggested by Folch 

 and Schneider,^^ w^ho based their opinion upon the probable presence of 

 serine in the cephalin fraction. This relationship was further supported 

 by the observation of Nord^^ that anaerobic bacteria decarboxylate serine 

 to yield ethanolamine. Levine and Tarver,*^ and Arnstein,^^ further con- 

 firmed this reaction by proving that serine labeled in the /3 position with 

 Qii gives rise to |8-labeled ethanolamine. 



c. Degradation of Ethanolamine in the Animal Body. Undoubtedly, 

 the major metabolic route for ethanolamine is its conversion to choline. 



'2De W. Stetten, Jr., J. Biol. Chem., 138, 437-438 (1941); I40, 143-152, cxxvii 

 (1941). 



" D. Shemin, J. Biol Chem., 162, 297-307 (1946). 



'^ P. D. Goldsworthy, T. Winnick, and D. M. Greenberg, J. Biol. Chem., 180, 341- 

 343 (1949). 



'5 T. Winnick, I. Moring-Claesson, and D. M. Greenberg, /. Biol. Chem., 175, 127- 

 132 (1948). 



'6 P. Siekevitz, T. Winnick, and D. M. Greenberg, Federation Proc, 8, 250 (1949). 



" P. Siekevitz and D. M. Greenberg, J. Biol. Chem., 180, 845-856 (1949). 



'8 W. Sakami, J. Biol. Chem., 176, 995-996 (1948). 



■>^ J. Folch and H. A. Schneider, J. Biol. Chem.., 137, 51-62 (1941). 



80 F. F. Nord, Biochem. Z., 95, 281-285 (1919). 



8' M. Levine and H. Tarver, /. Biol. Chem., 184, 427-436 (1950). 



82 H. R. V. Arnstein, Biochem. J., 48, 27-32 (1951) 



