Semin Liver Dis. 2004 Aug;24(3):317-325. Related Articles, Links
Alcohol and Iron.
Tavill AS, Qadri AM.
Professor of Medicine and Nutrition; Consultant Hepatologist.
Iron in its free ferrous and ferric states may serve as a physiological
regulator of normal intracellular functions but can be a double-edged sword
when linked to several pathways of cellular toxicity. In particular, oxidative
stress-induced cytotoxicity leading to both necrosis and apoptosis (so-called
necrapoptosis) may be promoted by increased intracellular free iron. When
hepatocyte iron accumulates to excess in clinical alcohol abuse or in an
experimental, combined model of iron and alcohol hepatotoxicity, there is
evidence for synergy among the putative pathways of oxidative stress. Just how
excess hepatocyte iron accumulates in alcohol excess is unknown, but when the
usual safe harbor for intracellular iron, namely the endosomal-lysosomal
compartment, is compromised, it becomes a potent source of free, chelatable
pro-oxidant iron. In this regard excess iron in alcohol-induced liver damage
and alcohol excess in iron-overload disease are powerful cocktails promoting
subcellular organelle damage leading to cell death and fibrogenesis. In some
experimental circumstances, only the combined insults of both alcohol and iron
overload are capable of inducing cell injury and fibrogenesis. There are
clinical examples for such relative resistance to each hepatotoxin presented to
the liver in isolation that lend support to this concept of synergy of
pro-oxidant pathways of liver injury.
PMID: 15349808 [PubMed - as supplied by publisher]
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