A long-term study of the interaction between iron and alcohol in an animal model of iron overload
Olynyk, J., Hall, P., Reed, W., Williams, P., Kerr, R. and Mackinnon, M. (1995) A long-term study of the interaction between iron and alcohol in an animal model of iron overload. Journal of Hepatology, 22 (6). pp. 671-676.
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Background/Aims: The hypothesis that chronic alcohol ingestion potentiates iron-associated liver injury was investigated in the ‘carbonyl iron-overload rat model’.
Methods: Newborn male and female Wistar-Furth rats (seven per group) were used to investigate iron-alcohol interaction over a 26-week period. Groups 1 and 2 were iron loaded from birth, while the others received normal diet. At 10 weeks all rats commenced Lieber-DeCarli liquid diet; additional treatments were: group 1 6 g carbonyl iron/1000 ml diets plus alcohol; group 2 carbonyl iron in the liquid diet; group 3 alcohol in the liquid diet; group 4, the controls, received liquid diet only.
Results: This study confirmed our previous observation that iron-loading from birth resulted in grade III–IV siderosis, in both male and female rats, and caused fibrosis associated with periportal macrophages. Alcohol-feeding, in addition to iron-feeding for 26 weeks significantly lowered the hepatic iron concentration in both male and female rats compared to those fed iron only (p<0.05). Alcohol feeding did increase hepatic fibrosis in the iron-loaded animals. However, serum alanine aminotransferase activity was significantly higher in the iron-alcohol group than in the other groups (p<0.05).
Conclusions: Thus, contrary to expectation, chronic alcohol feeding failed to potentiate hepatic fibrosis in iron-overloaded rats, although there was rather more hepatocyte necrosis, and the serum alanine aminotransferase activity was significantly higher in the iron-alcohol group than in the other groups.
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