FUNCTION 



precursors, but A. H. Smith and C. E. Meyer ^^ claimed that the 

 reduced citric acid excretion in vitamin B^ deficiency was merely the 

 result of a lower intake of food and not a direct result of the absence 

 of aneurine. 



Atnino-acid Metabolism 



The connection between aneurine and amino acids is even more 

 obscure, although rats receiving 5 fig. of aneurine per day were said 

 to utilise protein more efficiently than rats receiving half this amount. ^^ 

 When extra phenylalanine was administered to vitamin B^-deficient 

 rats, phenylpyruvic acid was found in the urine,^^ but no evidence is 

 available ^^ to suggest that aneurine-deficient rats are less able 

 than normal rats to metabolise either phenylalanine or tyrosine. On 

 the other hand, it has been claimed ^^ that in vitamin B^ deficiency 

 there is an increased enzymatic degradation of histidine due to a 

 disturbance of the intermediary carbohydrate metabolism, whilst the 

 administration of aneurine to normal rats has been said ^* to reduce 

 the excretion of histidine ; this returned to normal on stopping the 

 administration of aneurine. An attempt has also been made ^^ to 

 associate aneurine with transamination, as it had been found that 

 tissues from vitamin Bi-deficient rats were much less effective than 

 tissues from normal rats in transferring the amino group from 

 L-glutamic acid to pyruvic acid. It is now known, however, that 

 this reaction is brought about by a coenzyme that contains, not 

 aneurine, but pyridoxine (see page 333). 



Oxaloacetic Acid 



The hypothesis that cocarboxylase catalyses the formation of 

 oxaloacetic acid is apparently directly opposed to the results of L. O. 

 Krampitz and C. H. Werkman,^^ who prepared from Micrococcus 

 lysodeikticus an enzyme that catalysed the reverse of reaction (6). 

 This decarboxylation required magnesium ions, but not cocarboxylase 

 or aneurine. Moreover, contrary to Smyth's observations with 

 Staphylococcus, oxaloacetic acid did not replace aneurine in the dis- 

 mutation of pyruvate with a culture of M. lysodeikticus from which 

 cocarboxylase and magnesiimi had been removed. 



Further data of this type were reported by J. H. Quastel and 

 D. M. Webley,^^ who worked with vitamin B^-deficient propionic acid 

 bacteria. They found that the oxidation of acetate and propionate 

 was accelerated by aneurine only in presence of magnesiiun and 

 potassium ions, whereas the oxidation of pyruvate was accelerated by 

 aneurine alone and not by magnesium or potassium ions alone. The 



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