The Role of B6-Deficiency in the Tryptophane-Niacin Relationships in Rats

Rosen, Fred S.; Huff, Jesse W.; Perlzweig, W. A.

doi:10.1093/jn/33.5.561

Cited by 56 publications

(11 citation statements)

References 10 publications

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“…The effect of the organism on compounds containing the indole nucleus, especially tryptophan, was determined because of the numerous references in the literature that tryptophan was a precursor of nicotinic acid in the metabolism of a number of genera (Haskins & Mitchell, 1949;Rosen, Huff & Perlzweig, 1946). Table 4 gives the results obtained with indolylpropionic acid and with L-tryptophan.…”

Section: Obtainedmentioning

confidence: 99%

The oxidation of nicotinic acid by Pseudomonas fluorescens

Pinsky

Michaelis

1952

Biochemical Journal

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The ability of certain bacterial species to oxidize nicotinic acid was first reported by Allinson (1943) who used suspensions of a Pseudomonas culture originally isolated by Dubos & Miller (1937). Nicotinic acid was degraded by suspensions prepared from cultures grown only in the presence of this compound. These suspensions failed to attack nicotinamide, coramine or nicotinuric acid. Allinson concluded that this oxidation was an adaptive feature of the organism. A short time later, Koser & Baird (1944) isolated strains of Pseudomonas fluore8cens and Serratia narcescens which were able to grow in a nicotinic acid medium. These strains did not attack isonicotinic acid, picolinic acid or pyridine. There was no growth or poor growth on nicotinamide, quinolinic acid or ethyl nicotinate. Nicotinethylamide and nicotindiethylamide supported growth to a very slight extent. Nichol & Michaelis (1947) suggested that an oxidase was responsible for the destruction of the nicotinic acid. Certain inhibitors were able to interfere drastically with the ability of bacterial suspensions to utilize nicotinic acid. These included sodium azide, hydroxylamine hydrochloride, octan-2-ol, laurylpyridinium chloride and toluene. The experiments reported below were designed to elucidate further, by means of Warburg respiration technique, the utilization of nicotinic acid as a source of carbon and nitrogen by Ps. fluorescens. A number of nicotinic acid analogues were tested with a view to finding intermediates and thereby outlining the possible metabolic route. In addition, inhibitors were used to characterize the enzyme. system. EXPERIMENTAL Organism. The organism used was Ps. fluorescens 30 of Koser & Baird (1944), which was found by Nichol & Michaelis (1947) to be the most active of the strains tested. Media andsuspensions. The broth medium, the agar slopes and suspensions of resting bacterial cells were prepared as outlined by Nichol &A Michaelis (1947). In the media, apart from the agar, the only source of C and N was nicotinic acid.

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Section: Obtainedmentioning

confidence: 99%

The oxidation of nicotinic acid by Pseudomonas fluorescens

Pinsky

Michaelis

1952

Biochemical Journal

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“…The suggestion that conversion of tryptophane into nicotinic acid in the rat was inhibited by indole-3-acetic acid (159) has not been substantiated by further experiments (160,161,162).…”

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confidence: 95%

Metabolic Inhibitors

Winzler¹

1949

Annu. Rev. Biochem.

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This review has been limited to a consideration of those meta bolic inhibitors which exert their effects by virtue of their struc tural similarity to compounds playing a role in metabolism and growth. Previous reviews by Woolley, by Welch, and by Roblin (1 to 6) have shown the concept of competitive antagonism toward essential metabolites by compounds of similar structure to be so well established as to require little further justification.General considerations.-The high hopes held forth for the development of new chemotherapeutic agents based on a rational application of this principle [e.g. (7)] have not yet been realized. However, such metabolic antagonists have already begun to be of service in elucidating metabolic functions of certain metabolites, as well as the pathways· of certain biosyntheses.A technique termed "inhibition analysis" has been applied in a series of papers by Shive and his co-workers to the study of the effect of a number of antagonists on bacterial growth (8 to 16). The procedure is based on the assumption that, if a metabolic inhibitor blocks a particular reaction and thus limits bacterial growth, addition of the product of the blocked reaction should permit growth. At higher concentrations of the antagonist, a second reaction may be inhibited, whereupon the addition of the product of the second reaction then still further reduces the sen sitivitity of the organism to the inhibitor.· A number of agents other than the competing metabolite itself may reverse the inhibiting effect of a metabolic antagonist, each giving characteristic changes in the inhibition index and showing characteristic competitive or noncompetitive behavior (16).That too facile interpretation of the results of inhibition analysis is possible was pointed out by Hitchings et al. (17), when. it was observed that an entirely abnormal compound, S-bromouracil, was implicated as a metabolic product of a reaction in the growth of Escherichia coli inhibited by S-nitrouracil. Other difficulties m 1 Annu. Rev. Biochem. 1949.18:535-558. Downloaded from www.annualreviews.org Access provided by University of California -Davis on 02/03/15. For personal use only. Quick links to online content Further ANNUAL REVIEWS Annu. Rev. Biochem. 1949.18:535-558. Downloaded from www.annualreviews.org Access provided by University of California -Davis on 02/03/15. For personal use only. Annu. Rev. Biochem. 1949.18:535-558. Downloaded from www.annualreviews.org Access provided by University of California -Davis on 02/03/15. For personal use only.

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“…4 The influ¬ ence of corn grits in the diet has been ameliorated by use of dextrose or dextrin as a source of carbohydrate, which suggests that the metabolism of micro-organisms in the intestine may play a part in the phenomenon.5 Using the excretion of nicotinic acid and of N-methyl nicotinamide in the urine as a criterion, Rosen and co-workers 6 showed with this criterion that the same relationship exists between tryptophane and nicotinic acid. Later it was shown that human beings behave like laboratory animals with respect to a diminished output of the metabolites of nicotinic acid when a deficiency of nicotinic acid exists and its correction with tryptophane.7 On this basis, an amino acid imbal¬ ance produced by the administration of phenylalanine or threonine to rats gave evidence of interference with nicotinic acid-tryptophane metabolism, and the intra¬ venous route was as effective as the oral.8…”

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confidence: 99%

The Relationship of Tryptophane and Nicotinic Acid

1949

JAMA

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The name of Dr. Joseph Goldberger inevitably comes to mind in any discussion of the causation, prevention and cure of pellagra. He pioneered in the attempts to associate the appearance of the disease with causative nutritional factors; as he continued his studies he repeatedly showed the parallelism between presence or absence of pellagra and differences in the diet of the persons under examination. Particularly was the consumption of proteins of recognized superior biologic value regularly associated with the absence of the disease. In 1937 Elvehjem and his co-workers 1 demonstrated that nicotinic acid prevented and cured the canine analogue of human pellagra, and its efficacy in treating pellagra in man was promptly demonstrated.2 The earlier suggestion that protein of high nutritional value exerted a favorable effect on human pellagra and the discovery of the curative properties of nicotinic acid were partially harmonized by the observation that, in the rat, growth is retarded if corn grits are added to an experimental diet low in nicotinic acid and that either nicotinic acid or tryptophane brings about resumption of growth.3The foregoing observations suggest a more or less close relationship between protein and nicotinic acid in nutrition; indeed, hydrolyzed fibrin and gelatin both act like corn grits in retarding growth and glycine, and a mixture of amino acids simulating completely hydrolyzed casein will also have this effect.4 The influ¬ ence of corn grits in the diet has been ameliorated by use of dextrose or dextrin as a source of carbohydrate, which suggests that the metabolism of micro-organisms in the intestine may play a part in the phenomenon.5 Using the excretion of nicotinic acid and of N-methyl nicotinamide in the urine as a criterion, Rosen and co-workers 6 showed with this criterion that the same relationship exists between tryptophane and nicotinic acid. Later it was shown that human beings behave like laboratory animals with respect to a diminished output of the metabolites of nicotinic acid when a deficiency of nicotinic acid exists and its correction with tryptophane.7 On this basis, an amino acid imbal¬ ance produced by the administration of phenylalanine or threonine to rats gave evidence of interference with nicotinic acid-tryptophane metabolism, and the intra¬ venous route was as effective as the oral.8The rat is ordinarily able to synthesize enough nicotinic acid to maintain its physiologic well-being; however, when corn grits are added to a ration poor in nicotinic acid, the coenzyme content of liver, volun¬ tary muscle and brain is decreased.9 The vital part played by these enzymes in tissue oxidation suggests the gravity of the situation in which a widely used food can, through an amino acid imbalance from its protein of modest biologic value, cause this deep-seated alteration of usual physiologic chemical reactions. Fur¬ ther investigation of the interrelations of the known causative factors in the production of nicotinic acid deficiency is warranted by the considerable importance ...

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The Role of B6-Deficiency in the Tryptophane-Niacin Relationships in Rats

Cited by 56 publications

References 10 publications

The oxidation of nicotinic acid by Pseudomonas fluorescens

The oxidation of nicotinic acid by Pseudomonas fluorescens

Metabolic Inhibitors

The Relationship of Tryptophane and Nicotinic Acid

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