In animal studies, prophylaxis with quercetinameliorated ethanol-stimulated mitochondrial dysfunction manifested by decreased membrane potential and by induced permeability transition though suppressing glutathione depletion, enzymatic inactivation of manganese superoxide dismutase, and glutathione peroxidase, ROS overgeneration, and lipid peroxidation in mitochondria. Quercetin, thus, may protect rat, especially hepatic mitochondria, from chronic ethanol toxicity through its hypolipidemic effect and antioxidative role, highlighting a promising preventive strategy for ALD by naturally occurring phytochemicals [21, 22] .