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dc.contributor.authorNjagi, E.N.M.
dc.contributor.authorBender, D. A.
dc.date.accessioned2014-07-22T09:11:28Z
dc.date.available2014-07-22T09:11:28Z
dc.date.issued1990-01
dc.identifier.citationExperimental Parasitology Volume 70, Issue 1, January 1990, Pages 43–54en_US
dc.identifier.issn0014-4894
dc.identifier.other1090-2449
dc.identifier.urihttp://ir-library.ku.ac.ke/handle/123456789/10539
dc.descriptionDOI: 10.1016/0014-4894(90)90084-Pen_US
dc.description.abstractIn mice, infection with 20–30 cercariae of Schistosoma mansoni resulted in a considerable reduction in the formation of 14CO2 from [14C]tryptophan. Infected animals excreted significantly lower amounts of kynurenine, kynurenic acid, and methyl pyridone carboxamide than did uninfected controls. There was no difference in the ability of hepatocytes isolated from infected or control animals to metabolise [14C]tryptophan. Hepatocytes from infected animals synthesized less NAD(P), but more niacin and N1-methyl nicotinamide from tryptophan. They showed no greater accumulation of kynurenine metabolites than did cells from control animals. The hepatocyte content of pyridoxal phosphate and the erythrocyte aspartate aminotransferase activation coefficient were the same in both groups of mice, suggesting that infection with S. mansoni does not deplete vitamin B6. The impairment of tryptophan metabolism in vivo was apparently not due to impaired hepatic metabolism. Rather, it seems likely that the parasites or their eggs take up tryptophan avidly from the host's circulation. Studies of parasite and egg metabolism of tryptophan may suggest novel approaches to the chemotherapy Of bilharzia.en_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.subjectSchistosoma mansonien_US
dc.subjectTryptophan metabolismen_US
dc.subjectNiacin synthesisen_US
dc.subjectVitamin B6en_US
dc.titleSchistosoma mansoni: Effects on tryptophan metabolism in miceen_US
dc.typeArticleen_US


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