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Effects of vitamin E deficiency on hepatic mitochondrial lipid peroxidation and oxidative metabolism in rats with chronic dietary iron overload

✍ Scribed by Bruce R. Bacon; Robert S. Britton; Rosemary O'Neill

Publisher: John Wiley and Sons
Year: 1989
Tongue: English
Weight: 799 KB
Volume: 9
Category: Article
ISSN: 0270-9139
DOI: 10.1002/hep.1840090309

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✦ Synopsis

In both hereditary hemochromatosis (HHC) and in the various forms of secondary hemochromatosis, there is a pathological expansion of total body iron stores, due mainly to an inappropriate increase in absorption of dietary iron (1-3). The liver is the major recipient of this excess absorbed iron, and after several years of high tissue iron concentration, portal fibrosis and eventually cirrhosis develop (1-5). Clinical evidence for toxicity to the liver due to iron has been provided by studies of patients with HHC (4, 6, 7), African iron overload (8, 9) and secondary hemochromatosis due to p-thalassemia

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