In a CLP-induced sepsis model, excessive ROS products such as superoxide (O2−) and H2O2 are metabolized by SOD, CAT, and GSH-Px, the major antioxidants that protect cytosolic organelles from toxic free radicals during oxidative stress.11 Similar to our results, recent studies reported that SOD and CAT levels decreased during CLP-induced sepsis in the affected tissues.23,24 Our data demonstrated that the administration of NR in the CLP septic group increased antioxidant enzyme activities. The gene discussed is SOD1; the disease is Sepsis.