FUNCTION 



These results have not been conhrmed, and R. D. Hawkins ^'^ could 

 find no increase in the activity of either true cholinesterase or pseudo- 

 cholinesterase on incubating the plasma of rats or dogs with folic acid 

 or on administering folic acid to dogs or men. Dinning et al?-^ suggest 

 that pteroylglutamic acid may function in a choline oxidase system, 

 since the livers and kidneys of Aminopterin-treated monkeys were 

 virtually devoid of choline oxidase, as were the livers and kidneys of 

 monkeys fed a pteroylglutamic acid-deficient diet. 



Catalytic hydrogenation of vitamin Be yielded a dihydro-compound, 

 which was readily oxidised to the parent compound, and it was sug- 

 gested that vitamin Be, like riboflavine, might function in an oxidation- 

 reduction enz5niie system. ^ 



It appears probable, indeed, that pteroylglutamic acid influences 

 tyrosine oxidation, because liver slices from pteroylglutamic acid- 

 deficient rats showed a decreased ability to oxidise tyrosine compared 

 with livers from normal rats,^ and the reduced oxygen uptake was 

 increased when pteroylglutamic acid was added in vitro. The ability 

 to oxidise tyrosine was also lower than normal in liver slices from 

 rats given Aminopterin, but in this instance no effect was observed 

 on the addition of pteroylglutamic acid in vitro. Aminopterin in vitro 

 had no effect on tyrosine oxidation by normal liver slices. It is 

 known that the amount of phenolic compounds in the urine is increased 

 in pernicious anaemia.* Scorbutic guinea-pigs also excreted large 

 amounts of tj^osine-like compounds, up to 45 % of a 450-mg. dose of 

 tyrosine being eliminated in the urine ; the administration of pteroyl- 

 glutamic acid or ascorbic acid produced a marked drop in the amount 

 of tyrosine excreted.^ Premature infants fed cows' milk but no 

 ascorbic acid excreted significant amounts of phenolic substances, and 

 in some instances this was decreased on administration of pteroyl- 

 glutamic acid, although the response was more marked and more 

 regular when ascorbic acid was given. ^° 



7-Methylfolic acid inhibited tyrosine decarboxylase only in very 

 high concentrations, although 7-methylfolic acid and pteroylaspartic 

 acid inhibited dopa decarboxylase and the inhibition was nullified by 

 folic acid.^ On the assumption that folic acid was connected with 

 the decarboxylation of tyrosine, which they presumed to be the first 

 step in the formation of adrenaline, Martin et al.'^ tested the hypo- 

 tensive action of 7-methylfolic acid. The fact that it proved to be a 

 powerful depressor is presumptive evidence in favour of the view that 

 folic acid is concerned with tyrosine decarboxylation. 



On the other hand, folic acid appears to have other functions. 

 Reference has already been made (page 517) to the theory, first 

 advanced by J. L. Stokes,^ that folic acid is responsible for the syn- 

 thesis of thymine. This is supported, not only by the observation 



527 



