Another important consequence of chronic alcohol consumption is oxidative stress, which has been defined as an imbalance between production and neutralization of reactive oxygen species (ROS). This pathologic buildup of ROS is thought to play an important role in the development of the alcoholic lung phenotype (Guidot and Hart, 2005). In animal models, chronic alcohol ingestion decreases glutathione (GSH), an important cellular antioxidant in the alveolar space (Bechara et al., 2005;Brown et al., 2001;Holguin et al., 1998). Synthesis of GSH depends on cysteine (Cys), and there is recent evidence that Cys and its oxidized counterpart cystine (Cyss) function as an important extracellular redox pair, while GSH and its oxidized form, glutathione disulfide (GSSG), operate more at the intracellular level (Iyer et al., 2009). Experimental models have shown that many of the detrimental effects of chronic alcohol consumption can be reversed with correction of this imbalanced redox state (Garcia-Ruiz et al., 1995;Zhou et al., 2005). Antioxidant defenses, of which Cys and GSH are just two components, are vital for cellular protection against oxidative stress. When faced with such stresses, cells respond
