Summary
An increasing number of studies have shown that hepatic lipid peroxidation and depletion of the liver content of antioxidants is evident in experimental animals exposed to ethanol, suggesting the possible involvement of oxidative damage in the pathogenesis of some of the toxic effects of alcohol. Recent findings demonstrate that hydroxyethyl radicals are generated during ethanol metabolism by the alcohol-inducible form of cytochrome P-450 (CYP2E1) and that human liver microsomes are similary capable of producing ethanol-derived radicals. These intermediates, along with reactive oxygen species, also produced by CYP2E1, can be regarded as possible causes of the stimulation of lipid peroxidation, detectable in liver biopsies and in the blood of patients suffering from alcohol-related liver diseases.
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© 1993 Birkhäuser Verlag Basel/Switzerland
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Albano, E., Clot, P., Tabone, M., Aricò, S., Ingelman-Sundberg, M. (1993). Oxidative Damage and Human Alcoholic Liver Diseases. Experimental and Clinical Evidence. In: Poli, G., Albano, E., Dianzani, M.U. (eds) Free Radicals: from Basic Science to Medicine. Molecular and Cell Biology Updates. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-9116-5_27
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DOI: https://doi.org/10.1007/978-3-0348-9116-5_27
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