A Spectrophotometric Method for Estimating Formimino-glutamic and Urocanic acid

Chanarin, I.; Bennett, Myra C.

doi:10.1136/bmj.1.5270.27

Cited by 95 publications

(16 citation statements)

References 8 publications

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“…The difference between the simulated Vco and measured Vco was 0.36 ml per hour and is entirely explainable on the basis of normal endogenous CO production. The Vco in normal young male subjects averages 0.42 (SD ± 0.07) ml per hour (5 t In these patients we measured serum folic acid (17) and urine formiminoglutamic and urocanic acids after a histidine load (18 Vco was again 3.64 ml per hour, and measured 'Vco was 3.70 ml per hour. The average endogenous Vco found in anesthetized dogs is 0.18 (SD + 0.08) ml per hour (9).…”

mentioning

confidence: 99%

Endogenous carbon monoxide production in patients with hemolytic anemia.

Coburn¹,

Williams²,

Kahn³

1966

J. Clin. Invest.

151

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It is desirable in many studies to be able to rapidly measure rates of erythrocyte and hemoglobin destruction. Labeling techniques have been utilized for this purpose but have the disadvantage of requiring several days' to weeks to obtain the desired data plus the hazards of radioactive isotopes. Estimations of hemoglobin turnover from measurements of fecal bile pigment or serum bilirubin concentrations contain large sources of error (1). Studies in which bile pigment is collected via bile duct fistulas have been of value in animal experiments (2) but are -not usually possible in man, and subjects who have bile fistulas cannot be called normal. At the present time it appears that many in vivo investigations of red cell survival in patients with hemolytic disease are limited by the lack of a precise rapid method for detecting changes in the rate of red cell destruction.It has been shown previously (3-9) that CO is an in vivo catabolic by-product of hemoglobin and

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mentioning

confidence: 99%

Endogenous carbon monoxide production in patients with hemolytic anemia.

Coburn¹,

Williams²,

Kahn³

1966

J. Clin. Invest.

151

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“…The increase of urinary histidine derivatives is mainly due to the deficiency of metabolically available THE though their increase was found in patients not clearly related to folic acid deficiency as lupus erythematosus, rheumatoid arthritis (12), and bone tuberculosis (11). The depletion of THE can result from the defici ency in dietary folic acid, but also from inhibition of the enzyme, dihydrof olate reductase, necessary for the conversion of the vitamin to its active form.…”

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confidence: 99%

Clinical and Experimental Evaluation of Urinary Histidine Derivatives as an Index of Folic Acid Metabolism

Ishihara

1969

J. Vitaminol

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“…Urocanic acid was converted into Figlu in the presence of urocanase, and the Figlu transferase effected the transfer of the formimino group of Figlu to tetrahydrofolic acid giving 5-formiminotetrahydrofolic acid. The addition of HCl produced 5, 10-methenyltetrahydrofolic acid which was estimated spectrophotometrically at 350 mu (Chanarin and Bennett, 1962).…”

Section: Estimation Of Formiminoglutamic and Urocanic Acid Formiminomentioning

confidence: 99%

Histidine Metabolite Excretion and Serum Folate Levels

Leake

Bresland

1965

Aust J Exp Biol Med

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Summary.A histidine loading test was performed on 31 patients before and after saturation with folic acid. These results were compared with pre-treatment serum folate levels. Thirteen patients had normal serum folate levels and urinary histidine metabolite excretion; six patients with low serum folate showed high urinary histidine metabolite excretion which returned to normal after folic acid therapy. Five patients had low serum folate but did not excrete abnormal concentrations of histidine metabolites. Seven patients had normal serum folate but excreted high concentrations of histidine metabolites which were reduced to normal after folic acid therapy.INTRODUCTION.

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A Spectrophotometric Method for Estimating Formimino-glutamic and Urocanic acid

Cited by 95 publications

References 8 publications

Endogenous carbon monoxide production in patients with hemolytic anemia.

Endogenous carbon monoxide production in patients with hemolytic anemia.

Clinical and Experimental Evaluation of Urinary Histidine Derivatives as an Index of Folic Acid Metabolism

Histidine Metabolite Excretion and Serum Folate Levels

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