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By M L Anson; Kenneth Bailey; John T Edsall

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2. Possible Sources of Glycine Synthesized by Animal Tissues In considering glycine formation from nitrogenous precursors the direct utilization of two carbon atoms and the nitrogen atom of the precursor is implied. 'COzH The alternative mechanism involving the biosynthesis of each carbon 2 + 1 N donor 1 2 atom from a separate precursor, X C CY + CHzNHz*COZH, is unlikely and will not be discussed. I n both cases, amination is, of course, an essential step and a nonspecific nitrogen donor is assumed.

CHzNHz Acetic acid Ethanolamine Carbohydrate % C H ~ - C O - C O z H Pyruvic acid .. 1 CH? CHzNMe2 Betaine CHzOH. COzH Glycollic acid HO&. CHzNHMe Sarcosine IT? II,N*CO \c’ N I1 \c H R (R = ribose or ribose phosphate 4-Aminoimidazole5-carboxamide riboside (or ribotide) 1 + CHzOH. CH2NMes Choline I 1 ? L --j \ . i . COzH ---- - I 1 1( N H ~C. COJI ll I HN CHa Creatine I I NII-CO I I N . CH? II I Cj. 2. Reactions of glycine in animal metabolism. , 1947), and fungi (Neurospora: Tatum, 1949; Penicillium chrysogenum: Arnstein and Grant, 1954).

However, since serine and glycine are also required as intermediates for several other biosynthetic reactions, the combined dietary supply of these amino acids could not have been sufficient and endogenous synthesis must have occurred. The quantitative validity of experiments involving the feeding of toxic amounts of benzoate now seems in any case extremely doubtful. First, unexplained differences in the levels of benzoate required t o produce toxic symptoms have been reported. Thus, White (1941), in contrast to Griffith (1929), found that as much as 5 % of sodium benzoate was necessary to retard the growth of rats fed a 6 % casein diet, although no other toxic symptoms were observed.

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