IMR Press / FBL / Volume 4 / Issue 4 / DOI: 10.2741/albano

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Hydroxyethyl radicals in ethanol hepatotoxicity
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1 Department of Medical Sciences, University “A. Avogadro” of East Piedmont, Via Solaroli 17, 28100 Novara, Italy
2 Dept. of Pathology, Harbor-ULCA Medical Center, 1000W Carson St. Torrance, CA 90509, USA
3 Div. of Molecular Toxicology, Institute of Environmental Medicine, Karolinska Intitute, Box 210, S-171 77 Stockholm, Sweden
Front. Biosci. (Landmark Ed) 1999, 4(4), 533–540;
Published: 15 June 1999

Alcoholic patients and experimental animals exposed to ethanol display biochemical signs of oxidative damage, suggesting a possible role of free radicals in causing some of the toxic effects of alcohol. The use of electron spin resonance (ESR) spectroscopy associated with spin trapping technique has demonstrated that hydroxyethyl radicals are generated during ethanol metabolism by the microsomal monoxygenase system, involving the alcohol-inducible cytochrome P450 2E1 (CYP2E1). Recent observations in rats fed intragastrically with a high fat diet containing ethanol indicate that the formation of hydroxyethyl radicals is associated with stimulation of lipid peroxidation and development of liver damage. Moreover, by alkylating liver proteins, and particularly CYP2E1, hydroxyethyl free radicals are also capable of inducing the production of specific antibodies which can be observed in ethanol-fed animals as well as in patients abusing alcohol. Recent studies have demonstrated that hydroxyethyl radical-derived antigens are exposed on the plasma membranes of hepatocytes exposed to ethanol where are able to target antibody-dependent cell-mediated immunotoxic reactions towards liver cells. Thus, beside to contribute to alcohol-mediated oxidative damage, hydroxyethyl free radicals can contribute by immunological mechanisms to cause hepatocellular lesions associated with alcohol abuse.

Oxidative Damage
Cytochrome P4502E1
Alcoholic Liver Disease
Oxidative Injury
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