Oxidative stress and antioxidant defenses in ethanol-induced cell injury.
Although in the past several mechanisms and factors have been proposed to be responsible for alcoholic liver disease (ALD), at present the involvement of oxygen free radicals and consequently of oxidative stress has acquired remarkable credit. In numerous experimental studies it has been shown the occurrence of alcohol-induced generation of oxygen- and ethanol-derived free radicals through different pathways and from different sources. Mitochondria appear to be both an important source of reactive oxygen species (ROS) and also a primary target of ethanol-induced damage. The consistent induction of the mitochondrial antioxidant enzyme manganese superoxide dismutase (Mn-SOD) observed in experimental animals after acute and chronic ethanol administration has all the characteristics of a "stress response" to an oxidative insult.
Koch
Osvaldo R
OR
Departmento de Patologia, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina. orkoch@yahoo.com.ar
Pani
Giovanni
G
Borrello
Silvia
S
Colavitti
Renata
R
Cravero
Amerys
A
Farrè
Stella
S
Galeotti
Tommaso
T
D000818:Animals; D000975:Antioxidants / Q000502:physiology*; D000431:Ethanol / Q000009:adverse effects*; D006801:Humans; D008108:Liver Diseases, Alcoholic / Q000235:genetics / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology
D000975:Antioxidants; D016159:Tumor Suppressor Protein p53; D000431:Ethanol