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Urinary p-tyramine in hereditary tyrosinemia: II. Origin of urinary p-tyramine.

Abstract
1. A patient with hereditary tyrosinemia (tyrosinosis) was given oral loads of p-tyramine and tyrosine with and without medication (neomycin) to investigate the respective roles of intestinal bacteria and tissues in accounting for the origin of urinary p-tyramine. 2. The excretion of a high circulating level of p-tyramine following an oral load of p-tyramine in a patient with hereditary tyrosinemia (tyrosinosis) was as conjugated p-hydroxyphenylacetic acid (p-HPAA) and conjugated p-tyramine. 3. Both intestinal bacterial activity and tissue decarboxylation appeared to account for urinary p-tyramine in this patient following an oral load of tyrosine. 4. Sterilization of the gut by oral neomycin and a second load of oral tyrosine further supported a predominate role for tissue decarboxylation in the origin of urinary p-tyramine. 5. The data suggested that a major route of tyrosine metabolism in man may be via tissue decarboxylation of tyrosine.
AuthorsG N Hoag, A Hill, W Zaleski
JournalClinical biochemistry (Clin Biochem) Vol. 10 Issue 1 Pg. 26-8 (Feb 1977) ISSN: 0009-9120 [Print] United States
PMID837523 (Publication Type: Journal Article)
Chemical References
  • Tyrosine
  • Oxygenases
  • 4-Hydroxyphenylpyruvate Dioxygenase
  • Neomycin
  • Tyramine
Topics
  • 4-Hydroxyphenylpyruvate Dioxygenase (deficiency)
  • Administration, Oral
  • Adolescent
  • Amino Acid Metabolism, Inborn Errors (urine)
  • Diet
  • Female
  • Humans
  • Neomycin (therapeutic use)
  • Oxygenases (deficiency)
  • Tyramine (administration & dosage, metabolism, urine)
  • Tyrosine (metabolism)

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