THE METABOLISM OF l-TYROSINE IN INFANTILE SCURVY 1

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Attention has been drawn by Levine, Marples, and Gordon (1) to the relationship between ascorbic acid and the urinary excretion of aromatic amino acid intermediates by the normal premature male infant, both during periods of high protein intake and supplemental tyrosine and phenylalanine ingestion. To our knowledge, no reports have been forthcoming of similar studies with older, ascorbic acid depleted subjects.3 This communication is concerned with the metabolism of l-tyrosine in infantile scurvy. Observations have been made on the urinary excretion products, the serum content of both hydroxyphenyl compounds and amino acid nitrogen. Sealock and his co-workers (2) have demonstrated that the oral administration of l-tyrosine to scorbutic guinea pigs results in the urinary excretion of the amino acid and its two principal deaminated products, parahydroxyphenylpyruvic and parahydroxyphenyllactic acids. A proof that this metabolic disorder is primarily dependent upon the state of ascorbic acid depletion is afforded by the observation that the tyrosyluria (hydroxyphenyluria) is abolished when the vitamin is given orally or parenterally. Certain liver extracts are capable of modifying an induced tyrosyluria ( 1, 3), and recently Woodruff and Darby (4, 5) have indicated that pteroylglutamic acid (PGA) exerts a similar effect in the depleted guinea pig maintained on a basal scorbutogenic diet with supplements of l-tyrosine. By the administration of PGA to normal premature infants, Govan and Gordon (6) in several instances observed a diminution in the tyrosyluria