This result was consistent with other studies that showed the contribution of oxidative stress in the pathogenesis of cholestasis as a consequence of generation of CPZ cation radicals and/or metabolic activation of CPZ to quinoneimine derivatives [22] and decrease in hepatic super oxide dismutase SOD, glutathione peroxidase GPx, and glutathione reductase GR activity after EE administration [23]. Here, SOD1 is linked to cholestasis.