The influence of bactericidal agents and of the absence of <scp>l</scp>-ascorbic acid on the accumulation of hydroxyphenyl compounds in the large intestine of guinea pigs after the consumption of high doses of <scp>l</scp>-tyrosine

Painter, H. A.; Zilva, Sylvester Solomon

doi:10.1042/bj0430398

Cited by 3 publications

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“…The biochemical processes whereby the keto and hydroxy acids, resulting from the deamination of tyrosine, are eliminated in the urine, have received little attention in the literature, but it has been verified that their excretion is associated with a high hydroxyphenyl content of the gut, liver, kidney, muscle and blood, in the scorbutic guinea pig undergoing tyrosine feeding (20). The elevation in serum content of tyrosyl and amino acid nitrogen observed to occur in the scorbutic infant, corroborates the latter observation.…”

Section: ) Urinary Tyrosine Intermediatesmentioning

confidence: 99%

THE METABOLISM OF l-TYROSINE IN INFANTILE SCURVY 1

Morris¹,

Harpur²,

Goldbloom³

1950

J. Clin. Invest.

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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) established by dietary cow's milk protein. Several in vitro studies on the respiration of liver preparations with tyrosine as a substrate (7-9) tend to confirm that ascorbic acid, PGA, and certain liver fractions are concerned with the complete metabolism of tyrosine.The appearance of alkaptonuria during periods of high aromatic amino acid consumption has been noted in the albino rat (10) and in the scorbutic guinea pig ( 11 ), but the excretion of homogentisic acid by human subjects in a state of ascorbic acid depletion has not been reported.The present investigation is concerned with the effect of ascorbic acid, PGA and vitamin B12, on the urinary and serum tyrosyl content of several infants with clinical and preclinical scurvy during supplemental l-tyrosine feedings. METHODSUrine specimens were collected under toluene and stored at 4°C. Metaphosphoric acid was used in addition to toluene as a preservative when urinary ascorbic acid analyses were undertaken. Blood samples, when required, were obtained by internal jugular puncture approximately one and one-half hours after feeding. The sera were kept frozen until their amino acid nitrogen. and hydroxyphenyl content had been estimated. All colorimetric estimations were made with either a Coleman Junior spectrophotometer or an Evelyn photoelectric colorimeter. 1) Total Urinary Tyrosyl (Hydroxyphenyl) Compounds These were estimated by the method of Folin and Ciocalteau as modified by Medes (12) and adapted to the spectrophotometer at a wavelength of 465 muA. 2) Urinary Tyros...

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Section: ) Urinary Tyrosine Intermediatesmentioning

confidence: 99%

THE METABOLISM OF l-TYROSINE IN INFANTILE SCURVY 1

Morris¹,

Harpur²,

Goldbloom³

1950

J. Clin. Invest.

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The influence of l-ascorbic acid on the disappearance of the phenolic group of l-tyrosine in the presence of guinea pig-liver suspensions

Painter

Zilva

1950

Biochemical Journal

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The metabolism of tyrosine and phenylalanine in premature infants: the effect of large doses

Woolf

Edmunds

1950

Biochemical Journal

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Effects of a high-protein diet on premature infants were investigated by Levine, Marples & Gordon (1939 cf. Levine, Dann & Marples, 1943). These infants were fed diets containing 5 g. or more of milk proteins/kg. body weight/day in the absence of ascorbic acid. The excretion of p-hydroxyphenylpyruvic acid and p-hydroxyphenyllactic acid rose with increased protein intake and continued as long as the high protein diet was fed, but was prevented or abolished by giving ascorbic acid. These authors found that full-term infants did not excrete these two acids on a similar high-protein diet, but in both premature and full-term infants the excretion of these acids could be initiated (or increased if already present) by feeding a large dose (up to 1 g./kg. body weight) ofL-tyrosine or DL-phenylalanine, and thereafter the excretion of these acids continued while the child was fed a high-protein diet free from ascorbic acid.Work along somewhat similar lines with guinea pigs has been carried out by Sealock & Silberstein

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The influence of bactericidal agents and of the absence of l-ascorbic acid on the accumulation of hydroxyphenyl compounds in the large intestine of guinea pigs after the consumption of high doses of l-tyrosine

Cited by 3 publications

References 6 publications

THE METABOLISM OF l-TYROSINE IN INFANTILE SCURVY 1

THE METABOLISM OF l-TYROSINE IN INFANTILE SCURVY 1

The influence of l-ascorbic acid on the disappearance of the phenolic group of l-tyrosine in the presence of guinea pig-liver suspensions

The metabolism of tyrosine and phenylalanine in premature infants: the effect of large doses

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