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Oxidative Medicine and Cellular Longevity
Volume 3, Issue 3, Pages 178-185
http://dx.doi.org/10.4161/oxim.3.3.12288

Acetaldehyde Adducts in Alcoholic Liver Disease

1Department of Medicine, Rhode Island Hospital and the Alpert Medical School of Brown University, Providence, RI, South Africa
2Department of Pathology, Rhode Island Hospital and the Alpert Medical School of Brown University, Providence, RI, South Africa
3Department of Internal Medicine, University of Cape Town, Cape Town, South Africa

Received 12 April 2010; Revised 7 May 2010; Accepted 10 May 2010

Copyright © 2010 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Chronic alcohol abuse causes liver disease that progresses from simple steatosis through stages of steatohepatitis, fibrosis, cirrhosis, and eventually hepatic failure. In addition, chronic alcoholic liver disease (ALD), with or without cirrhosis, increases risk for hepatocellular carcinoma (HCC). Acetaldehyde, a major toxic metabolite, is one of the principal culprits mediating fibrogenic and mutagenic effects of alcohol in the liver. Mechanistically, acetaldehyde promotes adduct formation, leading to functional impairments of key proteins, including enzymes, as well as DNA damage, which promotes mutagenesis. Why certain individuals who heavily abuse alcohol, develop HCC (7.2–15%) versus cirrhosis (15–20%) is not known, but genetics and co-existing viral infection are considered pathogenic factors. Moreover, adverse effects of acetaldehyde on the cardiovascular and hematologic systems leading to ischemia, heart failure, and coagulation disorders, can exacerbate hepatic injury and increase risk for liver failure. Herein, we review the role of acetaldehyde adducts in the pathogenesis of chronic ALD and HCC.