The fate of nicotinamide in the mouse; Tissue metabolites☆

Chaykin, Sterling; Dagani, Michael; Johnson, Lane; Samli, Marqueta; Battaile, J.

doi:10.1016/0304-4165(65)90004-8

Cited by 52 publications

(28 citation statements)

References 16 publications

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“…This inhibition can be prevented by the addition of methionine to the diet or by a combination of choline plus homocystine in the diet (13). Apparently detoxification occurs through methylation of the nicotinamide to form N-methyl nicotinamide (4,6). This same mechanism may be prevalent in E. coli because isoniazid inhibition (which may result in nicotinic acid or nicotinamide accumulation, or both) is reversed by these same compounds.…”

Section: Resultsmentioning

confidence: 99%

Protection of Escherichia coli from Isoniazid Inhibition

Tritz

1974

Antimicrob Agents Chemother

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Inhibition of Escherichia coli by isonicotinic acid hydrazide (isoniazid) is a function of the initial cell concentration, concentration of antibiotic, and chemical composition of the medium. An initial concentration of 5 × 10 5 cells/ml in a minimal medium is inhibited by 1 mM isoniazid. The E. coli cells are protected from this inhibitory effect by a high concentration of cells in the medium. Protection is also obtained from vitamin-free Casamino Acids, methionine, or choline plus homocystine. However, nicotinic acid, nicotinamide, and pyridoxamine are not able to reverse the effect of isoniazid. Colonies arising on minimal medium supplemented with isoniazid are not due to selection of resistant mutants, because this resistance is transitory and not passed on to the daughter cells. It is hypothesized that this transitory resistance is a manifestation of the cells' ability to transfer the methyl group of methionine to either isoniazid or accumulated nicotinic acid and/or nicotinamide.

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Section: Resultsmentioning

confidence: 99%

Protection of Escherichia coli from Isoniazid Inhibition

Tritz

1974

Antimicrob Agents Chemother

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“…Urinary excretion of nicotinic acid and nicotinuric acid was observed in rat (1, 2), guinea pig, and hamster but not in mouse. Chaykin et al (5) reported that there are two types of mice: one can convert nicotinamide into nicotinic acid, and one cannot. None of the mice used here could convert nicotinamide into nicotinic acid.…”

Section: Hamstermentioning

confidence: 99%

“…Although there are two reports about catabolism of niacin in other rodents, guinea pig (4) and mouse (5), the precise data are not reported. So, we investigated the catabolic pathway of nicotinamide in mouse, guinea pig, and hamster to compare it with that in rat.…”

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confidence: 99%

Niacin catabolism in rodents.

Shibata¹,

Kakehi²,

Matsuo³

1990

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryUrinary excretion of nicotinamide and its metabolites in mouse, guinea pig, and hamster with a pharmacological amount of nicotinamide or N1-methylnicotinamide (MNA) was investigated to compare them with those of rat. In mouse, nicotinamide N-oxide was the most abundant metabolite, accounting for 35% of urinary excretion of nicotinamide and its metabolites, and followed by N1-methyl-2-pyridone -5-carboxamide (2-Pyr), 20%; nicotinamide, 18%; MNA, 16%; and N1-methyl-4-pyridone-3-carboxamide (4-Pyr), 11%. In guinea pig, 2-Pyr was the most abundant metabolite, accounting for 80% of urinary excretion, and was followed by MNA, 11%; nicotinamide, 3%; 4-Pyr , 3%; and nicotinamide N -oxide, 3%. In hamster, nicotinamide was the most abundant metabolite, accounting for 44%, and followed by 2-Pyr, 21%; nicotinamide N-oxide, 15%; MNA, 10%; and 4-Pyr , 10%. Urinary excretion of nicotinic acid and nicotinuric acid was not detected in mouse, guinea pig, and hamster. When a pharmacological amount of nicotinamide was intraperitoneally injected into mouse, the excretion of nicotinamide N-oxide increased to 79.7% of the nicotinamide metabolites, while those of MNA (4.9%), 2-Pyr (11.2%), and 4-Pyr (6.3%) decreased. Nicotinic acid and nicotinuric acid were again not detected. When a pharmacological amount of nicotinamide was intraperitoneally injected into guinea pig and hamster, the deamidated metabolites nicotinic acid and nicotinuric acid occupied significant percentages of the nicotinamide metabolites: 50.4% and 26.3%, respectively, in guinea pig; and 7.7% and 79.5%, respectively , in hamster. The ratio of 2-Pyr to 4-Pyr excretion did not change when nicotinamide or MNA was locaded into mouse , guinea pig, and hamster. From these results, the catabolism of nicotinamide in rodent is discussed .

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“…Both the methylated and the oxidized forms of NAM can be detected in the blood and urine of humans and rodents. Under normal conditions, the cytoplasmic clearance pathway predominates; however, pharmacologic doses of vitamin B 3 increase NAM N-oxide, which can become the most abundant NAM metabolite in mouse blood (Chaykin et al, 1965;Shibata et al, 1990;Stratford and Dennis, 1992). In humans, NAM N-oxide is detected after therapeutic doses of niacin for the treatment of hyperlipidemia (Menon et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

NicotinamideN-Oxidation by CYP2E1 in Human Liver Microsomes

2012

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Excess nicotinamide, a form of vitamin B 3 , is metabolized through two enzymatic systems and eventually excreted from the body. The first system starts with the methylation of nicotinamide by nicotinamide N-methyltransferase, which can subsequently be oxidized by aldehyde oxidase. The second enzymatic system oxidizes nicotinamide to nicotinamide N-oxide. It is located in the endoplasmic reticulum of hepatocytes but the precise enzyme is unknown. We have used human liver microsomes in combination with selective cytochrome P450 inhibitors, specific substrates, and antibodies to identify CYP2E1 as the main activity producing nicotinamide N-oxide. Our results suggest the potential use of nicotinamide N-oxide as a biomarker of CYP2E1 activity from urine or blood samples.

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The fate of nicotinamide in the mouse; Tissue metabolites☆

Cited by 52 publications

References 16 publications

Protection of Escherichia coli from Isoniazid Inhibition

Protection of Escherichia coli from Isoniazid Inhibition

Niacin catabolism in rodents.

NicotinamideN-Oxidation by CYP2E1 in Human Liver Microsomes

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