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Lipid Peroxidation and Associated Hepatic Organelle Dysfunction in Iron Overload

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Abstract

It has recently been recognized that genetic hemochromatosis (GH) is one of the most common inherited disorders. Approximately 0.1%–0.8% of whites of northern European ancestry are affected and the frequency of heterozygotes is thought to be about 5%–16% of the population [7, 12, 17, 20, 24, 34, 39, 43, 44, 53, 54]. In GH, there is an inappropriate increase in intestinal absorption of iron leading to progressive deposition of excess iron in parenchymal cells of the liver and several other organs [26, 28, 41, 47, 56]. The liver is the major recipient of the excess absorbed iron and after several years of high tissue iron concentrations, fibrosis and eventually cirrhosis develop [8, 38, 42, 56]. In addition, excess iron deposition in the liver is found in a variety of other disorders leading to secondary iron overload (e.g., thalassemia, chronic liver disease, porphyria cutanea tarda, sideroblastic anemia, African iron overload) [8, 26, 38, 41, 56].

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© 1992 Springer-Verlag Berlin Heidelberg

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Bacon, B.R., Britton, R.S., O’Neill, R. (1992). Lipid Peroxidation and Associated Hepatic Organelle Dysfunction in Iron Overload. In: Csomós, G., Fehér, J. (eds) Free Radicals and the Liver. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76874-3_7

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  • DOI: https://doi.org/10.1007/978-3-642-76874-3_7

  • Publisher Name: Springer, Berlin, Heidelberg

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