Hepatic steatosis has been widely recognized as an early and reversible consequence of excessive alcohol consumption [87]; pretreatment with PO results in the increased concentration of the hepatic antioxidant, GSH, and a concomitant increase in the GSH/GSSG ratio, as well as the activation of anti-oxidative enzymes glutathione reductase (GR) and SOD. Here, GSR is linked to Hepatic steatosis.