314 ASCORBIC ACID 



ascorbic acid with a similar effect. Painter and Zilva^*^ in in vitro experi- 

 ments reported essentially the same results with D-glucoascorbic acid as 

 with equivalent amounts of ascorbic acid, which tended to throw doubt 

 on the effect as being one of vitamin action. Rienits"^"'* published data, how- 

 ever, which indicated that L-ascorbic acid is specific and that D-ascorbic 

 acid and D-glucoascorbic acid had no effect. He showed by oxygen 

 consumption measurements and by determination of the disappearance of 

 hydroxyphenyl groups from liver slices that oxidation of tyrosine is related 

 to the ascorbic acid nutrition of the animal. 



The discrepancy in the response of liver slices and liver homogenates in the 

 oxidation of tyrosine is at least partially explainable by results reported by 

 Sealock's laboratory.^''^^'^'^ Sumerwell and Sealock^*"^ showed that a con- 

 siderably greater proportion of the ascorbic acid in the livers of scorbutic 

 animals, as compared to that in normal animals, is present in bound form 

 and much of it is not measured by the usual methods of assay. More re- 

 cently, Sealock et alr^'^" have shown that when the ratio of tissue to tyrosine 

 is large, as in the case of homogenates, sufficient ascorbic acid is present 

 even in scorbutic livers to cause oxidation of the tyrosine, whereas in the 

 liver slices the amount of the vitamin present is too small to oxidize the 

 tyrosine. Their results also showed that for completing the oxidation of 

 tyrosine the vitamin is needed only in extremely small amounts. Studies 

 with glucoascorbic acid, D-isoascorbic acid, and reductone, compounds re- 

 lated chemically and structurally to ascorbic acid, gave indication that it 

 is the enediol linkage which is responsible for the action of the vitamin as 

 a coenzyme in tyrosine oxidation. These are not compounds normally pres- 

 ent in living tissues. One of them, glucoascorbic acid, has been shown-^^^ to 

 produce a slight alleviation of scurvy symptoms when fed to animals sub- 

 sisting on a scorbutigenic diet. There are no ready explanations for this 

 type of response, but it would seem that the possibility should not be over- 

 looked that liver tissue may contain a factor which aids in the conversion 

 of a small amount of the compound to the L-ascorbic acid form. 



Recent results of Schepartz and NadeP^'^ with acetone powder prepara- 

 tions of guinea pig liver have demonstrated that the failure in tyrosine 

 metabolism in scorbutic animals, as indicated by a decrease in enzymatic 

 activity, is a result of vitamin C deficiency and not due to inanition. 



Woodruff and Darby^^^ showed that folic acid as well as ascorbic acid can 

 prevent the excretion of abnormal metabolites in scorbutic guinea pigs. 



"9 H. A. Painter and S. S. Zilva, Biochem. J. 46, 542 (1950). 



"oa K. G. Rienits, J. Biol. Chem. 182, 11 (1950). 



260b w. N. Sumerwell and R. R. Sealock, J. Biol. Chem. 196, 753 (1951). 



^si" W. G. Shafer, J. Dental Research 29, 831 (1942). 



"lb B. Schepartz and E. M. Nadel, Federation Proc. 11, 425 (1952). 



2" C. W. Woodruff and W. J. Darby, J. Biol. Chem. 172, 851 (1948). 



