In addition, use of tBHP in sham rats induced oxidative stress evidenced by increased renal H2O2 concentration (108.5±7.1 nmol/mg protein), TBARS level (2.02±0.16 nmol/mg protein) and decreased SOD level (28.3±3.9 U/mg protein) as compared to the sham-burned group (all P<0.01) (Fig. 4A–C), and thus led to significant tubular cell apoptosis (7.4±0.8%; P<0.01) (Fig. 3A) and renal dysfunction as assessed by elevated BUN (35.9±2.6 mg/dl; P<0.05) and creatinine (0.56±0.04 mg/dl; P<0.05) (Fig. 1C–D). This evidence concerns the gene SOD1 and Abnormal renal physiology.