| ironjustice@aol.com 2005-08-03, 5:55 pm |
| Alcohol. 2005 Apr;35(3):243-9. Related Articles, Links
Alcohol, iron-associated oxidative stress, and cancer.
Petersen DR.
Department of Pharmaceutical Sciences, Box C238, university of Colorado
Health Sciences Center, 4200 East 9th Avenue, Denver, CO 80262, USA.
Oxidative stress is recognized to play an important role in the
initiation and promotion events of carcinogenesis. Alcoholic liver
disease is associated with significant oxidative stress as well as the
hepatic accumulation of iron, a transition element also documented to
initiate oxidative stress. The combined prooxidant potential of ethanol
and iron is at least additive and possibly synergistic with respect to
inducing hepatocellular oxidative stress and antioxidant depletion. One
cellular consequence of sustained oxidative stress and redox imbalance
resulting from the combined actions of alcohol and iron is lipid
peroxidation, resulting in the production of aldehydic products such as
4-hydroxy-2-nonenal, which has been linked to site-specific mutations
of the p53 gene. In addition, the accumulation of iron in hepatic
macrophage isolated from laboratory animals chronically ingesting
alcohol is associated with activation of nuclear factor-kappa B and
production of tumor necrosis factor-alpha, providing a proinflammatory
cellular environment also favorable for initiation and promotion of
carcinogenesis. Consequently, there is persuasive evidence that the
potential of ethanol and iron to induce oxidative stress may be an
important pathogenic mechanism for the increased occurrence of
hepatocellular carcinoma in individuals with hepatic iron overload who
ingest alcohol.
PMID: 16054986 [PubMed - in process]
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