ABSTRACT
Reduced glutathione (GSH) is known to play a critical role in detoxication processes of cells, including hydroperoxide catabolism (GSH-peroxidase-glutathione disulfide (GSSG) reductase system), conjugation with electrophiles (GSH transferases), and direct interception of free radicals or quenching of excited states. 13 From this viewpoint, the relationship between GSH and ethanol has been extensively explored in the past years in connection with the development of an oxidative stress condition in the liver as a possible lesioninducing mechanism leading to alcoholic hepatic necrosis. 2 , 4 , 5 Cellular oxidative stress is a disturbance in the prooxidant/antioxidant balance in favor of the former, 6 which can be achieved by either an enhancement of oxidative reactions with production of reactive oxygen species, a diminution of antioxidant defenses, or both. Thus, an alteration in the GSH content of the liver by ethanol could represent a major component of oxidative stress in the tissue 2 and could also lead to an imbalance in the interorgan GSH homeostasis, as the liver appears to have a central role in supplying extrahepatic tissues with GSH or its component amino acids. 7
