VIII. KFFKCTS OF DEFICIENCY IN ANIMALS 313 



tissues in animals nmcli as in plants. The disappearance of the vitamin is 

 greater during periods of rapid growth. In the guinea pig, supplied daily 

 by injection with constant amounts (5 mg. per 100 g. of liody weight) of 

 ascorbic acid, less of the \'itamin in the urine is (>xcreted i)er iniit of body 

 weight by the young than l>y the full-grown animal, and the younger the 

 animal and the more rapitlly it glows, the smaller the amount excreted.-" 

 Part of the administered dose is held by the tissue, some is destroyed and 

 is accounted for chiefly as carbon dioxide, possibly some as oxalic acid in 

 the feces, and the remainder is excreted in the urine. The metabolic losses 

 of the vitamin may be due entirely to l)reakdown to carbon dioxide, oxalic 

 acid, and possibly other products.-* However, as pointed out previously, 

 the complete picture of the biochemical metabolism of ascorbic acid has 

 not been revealed. 



a. Proteins and Amino Adds 



Ascorbic acid plays an important role in intermediate protein metabolism, 

 particularly with respect to the oxidation of the aromatic amino acids, tyro- 

 sine and phenylalanine. The literature on the subject has recently been 

 reviewed by Woods. '^^ \Vhen the aromatic amino acids are fed in large 

 amounts to premature infants subsisting on cow's milk-*^ or to guinea pigs 

 on a diet lacking ascorbic acid, there is an excretion of abnormal metabolites 

 (p-hydroxyphenyllactic and p-hydroxyphenylpyruvic acids) in the urine. ^^ 

 Sealock et o/.^° showed also that guinea pigs receiving supplements of tyro- 

 sine or phenylalanine or their derivatives, and only maintenance amounts 

 of ascorbic acid, excreted homogentisic acid in amounts proportional to the 

 intake of ascorbic acid. Of a large series of phenylalanine and tyrosine 

 derivatives only L-phenylalanine, L-tyrosine, and phenylpyruvic acid 

 showed any dependence on the intake of ascorbic acid. The vitamin ap- 

 peared to function at a point prior to the formation of the tyrosine keto 

 acids. 2"*^ Investigations by Knox and LeMay-Knox^^^ have revealed the steps 

 in the oxidation of tyrosine in liver homogenates. The initial reaction is 

 a tyrosine-a-ketoglutarate transamination with the formation of glutamate 

 and p-hydroxyphenyl pyruvate. Addition of ascorbic acid to the mixture 

 had no efTect on the rate of deamination but affected notably the oxidation 

 of p-hydroxyphenyl pyruvate. The action of ascorbic acid appeared to be 

 chiefly one of continuing the oxidation of tyrosine to the formation of aceto- 

 acetate. These investigators reported also that isoascorbic acid could replace 



»" M. E. Reid, J. Nutrilion 35, 619 (1948). 



*" R. Woods, Borden's Rev. Nutrition Research 10, No. 7 (1949). 



"» S. Z. Levine, E. Marples, and H. H.' Gordon, Science 90, 620 (1939). 



2" D. H. Basinski and R. R. Sealock, J. Biol. Chem. 166, 7 (1946). 



"8 W. E. Knox and M. LeMay-Knox, Biochem. J. 49, 686 (1951). 



