IN THE year 1939 it was found that premature infants excreted the deaminated residues of tyrosine and phenylalanine when fed high protein diets low in vitamin C.1 Full-term infants behaved similarly when their high-protein diets were supplemented by tyrosine or phenylalanine.2 The administration of ascorbic acid led to consistent eradication of the hydroxyphenyluria (tyrosyluria). Liver extract decreased tyrosyluria in two of four premature infants and eliminated it in one full-term infant.
Independently, Sealock and Silberstein3 found a similar metabolic disorder in guinea pigs fed a scorbutic diet with supplements of l-tyrosine. The response of this hydroxyphenyluria to the administration of ascorbic acid, an anti-pernicious-anemia preparation (liver extract),4 or a variety of acidic substances5 suggested that many factors contribute to complete oxidation of tyrosine and phenylalanine.
Studies of the tyrosyluria of patients with pernicious anemia6 and of scorbutic individuals7 have shown that the