It is well known that ethanol alters phase II metabolism of xenobiotics agents [108]. Depletion of GSH reservoirs reduces the liver ability to withstand oxidative stress from altered redox equilibrium and to prevent lipids peroxidation as a result of ethanol ingestion. Dai et al. [10] and Gyamfi and Wan [109] demonstrated that GSH levels are reduced in wild-type mice after ethanol administration; this effect is exacerbated in RXR null mice [10, 109]. Compared to wild-type mice, hepatocyte RXRα-deficient mice have significant lower levels of SAM (a precursor for GSH synthesis) and GSH, which is further reduced after alcohol treatment [10, 11]. The Glutathione S-transferase (GSTs) is a multigene family of enzymes that bind GSH to xenobiotics agents facilitating theirs dissolution in the aqueous cellular and extracellular media, and, from there, out of the body.
