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dc.contributor.authorBender, DA
dc.contributor.authorNjagi, EN
dc.contributor.authorDanielian, PS
dc.date.accessioned2013-12-04T16:10:22Z
dc.date.available2013-12-04T16:10:22Z
dc.date.issued1990
dc.identifier.citationBr J Nutr. 1990 Jan;63(1):27-36.en_US
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/2317476
dc.identifier.urihttp://hdl.handle.net/11295/61836
dc.description.abstractVitamin B6 deficiency was induced in mice by maintenance for 4 weeks on a vitamin B6-free diet. Tryptophan metabolism was assessed by determining the urinary excretion of tryptophan metabolites, the metabolism of [14C]tryptophan in vivo and the formation of tryptophan and niacin metabolites by isolated hepatocytes. The vitamin B6-deficient animals excreted more xanthurenic acid and 3-hydroxykynurenine, and less of the niacin metabolites N1-methyl nicotinamide and methyl-2-pyridone-4-carboxamide, than did control animals maintained on the same diet supplemented with 5 mg vitamin B6/kg. After intraperitoneal injection of [14C]tryptophan, vitamin B6-deficient mice showed lower liberation of 14CO2 from [methylene-14C]tryptophan and [U-14C]tryptophan than did controls, indicating impairment of kynureninase (EC 3.7.1.3) activity. There was no difference between the two groups of animals in the metabolism of [ring-2-14C]tryptophan. Hepatocytes isolated from the vitamin B6-deficient animals formed more 3-hydroxykynurenine and xanthurenic acid than did cells from control animals, but also formed more NADP and free niacin.en_US
dc.language.isoenen_US
dc.publisherCambridgeen_US
dc.titleTryptophan metabolism in vitamin B6-deficient mice.en_US
dc.typeArticleen_US


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