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dc.contributor.authorKim, Jonghan
dc.contributor.authorBuckett, Peter D.
dc.contributor.authorWessling-Resnick, Marianne
dc.date.accessioned2013-12-13T20:21:33Z
dc.date.issued2013
dc.identifier.citationKim, Jonghan, Peter D. Buckett, and Marianne Wessling-Resnick. 2013. Absorption of manganese and iron in a mouse model of hemochromatosis. PLoS ONE 8(5): e64944.en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:11377981
dc.description.abstractHereditary hemochromatosis, an iron overload disease associated with excessive intestinal iron absorption, is commonly caused by loss of HFE gene function. Both iron and manganese absorption are regulated by iron status, but the relationships between the transport pathways of these metals and how they are affected by HFE-associated hemochromatosis remain poorly understood. Loss of HFE function is known to alter the intestinal expression of DMT1 (divalent metal transporter-1) and Fpn (ferroportin), transporters that have been implicated in absorption of both iron and manganese. Although the influence of HFE deficiency on dietary iron absorption has been characterized, potential effects on manganese metabolism have yet to be explored. To investigate the role of HFE in manganese absorption, we characterized the uptake and distribution of the metal in Hfe−/− knockout mice after intravenous, intragastric, and intranasal administration of 54Mn. These values were compared to intravenous and intragastric administration of 59Fe. Intestinal absorption of 59Fe was increased and clearance of injected 59Fe was also increased in Hfe−/− mice compared to controls. Hfe−/− mice displayed greater intestinal absorption of 54Mn compared to wild-type Hfe+/+ control mice. After intravenous injection, the distribution of 59Fe to heart and liver was greater in Hfe−/− mice but no remarkable differences were observed for 54Mn. Although olfactory absorption of 54Mn into blood was unchanged in Hfe−/− mice, higher levels of intranasally-instilled 54Mn were associated with Hfe−/− brain compared to controls. These results show that manganese transport and metabolism can be modified by HFE deficiency.en_US
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofdoi:10.1371/journal.pone.0064944en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660331/pdf/en_US
dash.licenseLAA
dc.subjectBiologyen_US
dc.subjectBiochemistryen_US
dc.subjectMetabolismen_US
dc.subjectBiological Transporten_US
dc.subjectTissue Distributionen_US
dc.subjectToxicologyen_US
dc.subjectNeurotoxicologyen_US
dc.subjectChemistryen_US
dc.subjectEnvironmental Chemistryen_US
dc.subjectPollutantsen_US
dc.subjectHeavy Metalsen_US
dc.subjectMedicineen_US
dc.subjectDrugs and Devicesen_US
dc.subjectPharmacokineticsen_US
dc.subjectDrug Absorptionen_US
dc.subjectDrug Distributionen_US
dc.titleAbsorption of Manganese and Iron in a Mouse Model of Hemochromatosisen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalPLoS ONEen_US
dash.depositing.authorKim, Jonghan
dc.date.available2013-12-13T20:21:33Z
dc.identifier.doi10.1371/journal.pone.0064944*
dash.contributor.affiliatedKim, Jonghan
dash.contributor.affiliatedBuckett, Peter
dash.contributor.affiliatedWessling-resnick, Marianne


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