Cellular iron metabolism in haemochromatotic macrophages

dc.contributor.authorIckinger, Claudia
dc.date.accessioned2018-07-25T13:53:59Z
dc.date.available2018-07-25T13:53:59Z
dc.date.issued1995
dc.descriptionA dissertation submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg, in fulfilment of the requirements for the Degree Master of Science in Medicine. Johannesburg, 1995en_ZA
dc.description.abstractHLA-linked haemochromatosis is the result of an inborn error of metabolism inherited as an autosomal recessive gene, closely linked to the HLA locus on chromosome six. In this condition iron absorption is inappropriately high leading to iron overload. Integral to the pathogenesis of this disorder and in contrast to other causes of iron overload, is the relatively modest accumulation of iron within cells of both the small intestine and the reticuloendothelial system and the excessive deposition of iron in parenchymal cells of the liver and other organs. This observation has led to the suggestion that the primary defect(s) could be present in either the gut, the liver, the reticuloendothelial system or all three. Abnormalities in iron uptake by cells, iron transport through and between cells and iron storage in cells have all been suggested as possible mechanisms responsible for the abnormal absorption and distribution of iron in haemochromatosis. Malfunction of the iron transport protein transferrin or its receptor could be responsible for abnormal distribution and iron loading while an abnormality of ferritin iron storage could explain why some cells appear to be unable to store iron and others are iron overloaded.en_ZA
dc.description.librarianIT2018en_ZA
dc.identifier.urihttps://hdl.handle.net/10539/25177
dc.language.isoenen_ZA
dc.subject.meshCells
dc.subject.meshIron Metabolism Disorders
dc.subject.meshHemochromatosis
dc.subject.meshMacrophages
dc.titleCellular iron metabolism in haemochromatotic macrophagesen_ZA
dc.typeThesisen_ZA
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