Tumour promotion versus tumour suppression in chronic hepatic iron overload.

摘要: Although iron-catalysed oxidative damage is presumed to be a major mechanism of injury leading cirrhosis and hepatocellular carcinoma in hemochromatosis, these events have been difficult recapitulate an animal model. In this study, we evaluated regulators hepatocarcinogenesis rodent model chronic iron overload. Sprague–Dawley rats were loaded with dextran over 6 months. Livers harvested analysed for markers stress, as well the following proteins: p53, murine double minute 2, Shc proteins p66, p52, p46; β-catenin, CHOP, C/EBPα Yes-associated protein. model, loading associated hepatocyte proliferation, indices are mildly increased tandem augmented antioxidant defenses. Alterations potentially favouring carcinogenesis included modest but significant decrease p53 levels increases p46 β-catenin compared control livers. Countering factors, iron-loaded livers demonstrated which has recently implicated development carcinoma, reciprocal increase Our results suggest that overload elicits both tumour suppressive tumour-promoting mechanisms liver. Copyright © 2015 John Wiley & Sons, Ltd.