Moreover, LPS-induced hepatocellular injury also elicits oxidative and nitrosative stress to result in an increase of oxidants like reactive oxygen (ROS) and nitrogen species and reduction of endogenous antioxidants such as superoxide dismutase (SOD) and glutathione (GSH) and elevation of malondialdehyde (MDA), which is implied in the pathophysiology of ALI [13,14]. This evidence concerns the gene SOD1 and acute respiratory distress syndrome.