442 VITAMIN Bi2 



of serine, or the a-carbon atom of glycine was shown to serve as a source 

 of the methyl carbon atom of choline or methionine. The extent to which 

 glycine and serine can replace choline for the methylation of homocystine 

 in the rat is at present ill-defined. A report by Arnstein and Neuberger"* 

 indicates that rats on a "labile-methyl-free" diet containing homocysteine 

 and vitamin B12 grew more rapidly in the presence of choline than in its 

 absence. 



Dinning and coworkers'^^ investigated the requirement of the rat for 

 "methylating" compounds in the treatment of leucopenia induced by feed- 

 ing a low-choline, low-methionine diet containing folic acid to rats. They 

 found that the requirement could be satisfied by betaine in the presence 

 of vitamin B12 or by methionine alone. For further studies, folic acid was 

 omitted from the basal diet and it was found that methionine was effective 

 in the absence of both vitamin B12 and folic acid, whereas choline or betaine 

 were effective only in the presence of these two vitamins. ^^^ 



It was suggested'^^' '^2 that vitamin B12 was a cof actor in the transforma- 

 tion of glycine into serine. However, a study of the radioactivity of the 

 /3-carbon atom of serine following the administration of a-C^'^-glycine to 

 rats did not indicate that vitamin B12 deficiency depressed this trans- 

 formation.^-^ The study showed that the deficiency lowered the rate of 

 conversion of glycine, serine, and formate into the CH3 group of methionine 

 and into all the carbons of choline. In pair-fed rats, vitamin B12 deficiency 

 slowed the passage of the carbon of a-labeled glycine into (1) the CH3 

 group of methionine in the viscera but not in the carcass and (2) the tri- 

 methylamine group of choline, but not the total molecule. The difference 

 between the results with full-fed rats and those with paired-fed rats makes 

 it evident that the interpretation of such results is difficult. 



The effects of deficiencies of vitamin B12 and folic acid on the formation 

 of glutathione in the intact rat were studied by Anderson and StekoV^* 

 who found that the deficiencies did not affect the incorporation of glycine 

 or cystine, respectively, into the glycine or cysteine components of gluta- 

 thione, but that either deficiency decreased the conversion of the a-carbon 

 of glycine into the cysteine and glutamic acid portions of the glutathione 

 molecule. 



'" H. R. V. Arnstein and A. Neuberger, Biochem. J. 48, ii (1951). 



"3 J. S. Dinning, C. K. Keith, and P. L. Day, J. Biol. Chem. 189, 515 (1951). 



'20 J. S. Dinning, C. K. Keith, and P. L. Day, J. Nutrition 43, 525 (1951). 



i'^' H. R. V. Arnstein and A. Neuberger, Biochem. J. 50, xxxviii, 1952. 



>22 J. A. Stekol, S. Weiss, and K. W. Weiss, Arch. Biochem. 36, 5, 1952. 



123 H. R. V. Arnstein and A. Neuberger, Biochem. J. 55, 259, 1953. 



124 K. I. Anderson and J. A. Stekol, J. Biol. Chem. 202, 611, 1953. 



