UTILIZATION OF PTEROYLGLUTAMIC ACID CONJUGATES IN THE IN VITRO SYNTHESIS OF L. CITROVORUM ACTIVITY<sup>1</sup>

Dietrich, L.S.; Monson, W. J.; Elvehjem, C. A.

doi:10.1021/ja01134a517

Cited by 9 publications

(5 citation statements)

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“…Urinary creatine and Nl-methylnicotinamide. The effect of pteroylglutamic acid (Fatterpaker et al , 1952aDietrich et al 1952;Dinning & Day, 1949) is confirmed (Table 3). Increased methylation of the extra nicotinamide ingested could be seen and is much less in the pteroylglutamic acid deficient animals than in replete ones.…”

Section: Resultsmentioning

confidence: 71%

Observations on the relationship between pteroylglutamic acid and nicotinamide metabolism

Marfatia

Sreenivasan

1955

Biochemical Journal

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Slightly depressed growth and fatty livers have been reported in rats fed moderate amounts of nicotinamide, together with a low protein diet (Handler & Danm, 1942; Handler & Bemheimn, 1943). The fatty livers were susceptible to the action of choline, while methionine was found to alleviate the growth inhibition. Since excess of nicotinamide is detoxicated and eliminated as urinary N1-methylnicotinamide, the observed toxicity of nicotinamide at unphysiological levels of feeding was attributed to forced methylation and consequent depletion of labile methyl reserves (Handler, 1944). In agreement with this, Handler observed no signs of toxicity as a result of ingestion of large quantities of nicotinamide by young rabbits or guinea pigs, neither of which species excrete NL-methylnicotinamide (Handler, 1944). Production of fatty livers by feeding excessive amounts of glycocyamine, cystine or homocystine have also been reported (du Vigneaud, Chandler, Moyer & Keppel, 1939; du Vigneaud, Chandler, Cohn & Brown, 1940; Stetten & Grail, 1942). More recently, it has been shown that, in the pyridine-fed rat, there is a decreased urinary excretion of creatine owing to a reduction of available methyl groups, pyridine being detoxi-cated as N-methylpyridinium hydroxide (Dinning, Keith, Parsons & Day, 1950). The known mediation of pteroylglutamic acid in biological methylations including the methylation of nicotinamide (Fatterpaker, Marfatia & Sreenivasan, 1951, 1952a, 1954; Dietrich, Monson & Elvehjem, 1952) suggested the present studies on its influence on the extent of depletion of methyl reserves in rat livers consequent on ingestion of excessive amounts of nicotinamide. The studies included observations on a number of other substances and enzymes expected to be influenced by changes in pteroylglutamic acid or available labile methyl compounds. Pteroylglutamic acid deficiency was induced in the first set of experiments by dietary means, while in the second series aminopterin feeding was used. In the first series, additional groups with choline supplementation were included. EXPERIMENTAL Methods Urinary excretions of creatine (Clark & Thompson, 1949), Nl-methylnicotinamide (Huff & Perlzweig, 1947) and total nicotinic acid (Swaminathan, 1946), liver N (Johnson, 1941), This work was aided by a grant from the Indian Council of Medical Research. Our thanks are due to Lederle Laboratories Inc. (New York), Chas. Pfizer and Co. Inc. (New York), Glaxo Laboratories Ltd. (Greenford), and Boots Pure Drug Co. Ltd. (Nottingham) for valuable gifts of chemicals.

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Section: Resultsmentioning

confidence: 71%

Observations on the relationship between pteroylglutamic acid and nicotinamide metabolism

Marfatia

Sreenivasan

1955

Biochemical Journal

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“…Since leucovorin is only half as active as the 'natural' CF occurring in horse liver (Keresztesy & Silverman, 1951;Cosulich, Smith & Broquist, 1952), microbiological assay values in terms of leucovorin were divided by two to give results as naturally occurring CF. For determination of FA and CF in liver, these organs were homogenized and autolysed as described by Dietrich, Monson, Gwoh & Elvehjem (1952). Values of 'unconverted FA' were obtained by subtraction of Strep.…”

Section: Resultsmentioning

confidence: 99%

The metabolism of pteroylglutamic acid by the rat

Guggenheim

Halevy

Neumann

et al. 1956

Biochemical Journal

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“…Koch and Hanke (76), working with rat blood as a source of xanthine oxidase, showed that CN-, hypoxanthine and adenine were powerful inhibitors of uric acid formation. Petering and Schmitt (113) reported on the inhibitory effects of simple pterins related to 6-PA. Dietrich et d. (35) reported that 6-PA inhibited the chick liver xanthine oxidase also. Kalckar and Klenow (70) first reported the inhibitory effect of synthetic PGA but later demonstrated that the effect waa probably due to contaminating &PA (71).…”

Section: In Vztromentioning

confidence: 96%

Chemistry and Biochemistry of Xanthine Oxidase

Renzo¹

1956

Advances in Enzymology - And Related Areas of Molecular Biology

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UTILIZATION OF PTEROYLGLUTAMIC ACID CONJUGATES IN THE IN VITRO SYNTHESIS OF L. CITROVORUM ACTIVITY¹

Cited by 9 publications

References 0 publications

Observations on the relationship between pteroylglutamic acid and nicotinamide metabolism

Observations on the relationship between pteroylglutamic acid and nicotinamide metabolism

The metabolism of pteroylglutamic acid by the rat

Chemistry and Biochemistry of Xanthine Oxidase

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UTILIZATION OF PTEROYLGLUTAMIC ACID CONJUGATES IN THE IN VITRO SYNTHESIS OF L. CITROVORUM ACTIVITY1

Cited by 9 publications

References 0 publications

Observations on the relationship between pteroylglutamic acid and nicotinamide metabolism

Observations on the relationship between pteroylglutamic acid and nicotinamide metabolism

The metabolism of pteroylglutamic acid by the rat

Chemistry and Biochemistry of Xanthine Oxidase

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UTILIZATION OF PTEROYLGLUTAMIC ACID CONJUGATES IN THE IN VITRO SYNTHESIS OF L. CITROVORUM ACTIVITY¹