N-Acetylcysteine and High-Dose Atorvastatin Reduce Oxidative Stress in an Ischemia-Reperfusion Model in the Rat Kidney

• High-dose atorvastatin has protective effects against oxidative stress and inflammation in a rat kidney model of ischemia-reperfusion injury.
• High-dose atorvastatin reduces myeloperoxidase levels and increases scavenger activity of catalase and glutathione peroxidase.
• N-Acetylcysteine has a moderate influence on oxidative stress, and our results do not support the hypothesis of a synergistic effect of N-acetylcysteine and high-dose atorvastatin in protecting against oxidative stress.

ObjectiveTo investigate the effects of N-acetylcysteine (NAC) and high-dose atorvastatin (ATOR) in reducing oxidative stress in a rat kidney model of ischemia-reperfusion injury.MethodsForty female rats underwent clamping of the left renal artery for 30 minutes, followed by reperfusion. The effects of pre-ischemic administration of NAC and/or ATOR were evaluated within 4 groups: a) control (no NAC, no ATOR); b) NAC (intraperitoneal NAC administration); c) ATOR (oral ATOR administration); and d) NAC+ATOR (both drugs). Oxidative stress was assessed by measuring the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and myeloperoxidase (MPO). Post–ischemia-reperfusion injury was evaluated by means of renal histology.ResultsNAC, ATOR, and NAC+ATOR in rats showed lower MPO (P < .05) and higher GPx activity (P < .05) versus control; SOD activity was lower in NAC versus ATOR (P < .05). No difference among groups was found at histology. However, a lower rate of tubular ischemic lesions was evident in NAC+ATOR versus control (P = .07).ConclusionsAtorvastatin pretreatment provides protection against oxidative stress in a rat kidney model of ischemia-reperfusion injury, reinforcing the evidence of a beneficial effect of statins beyond their cholesterol-lowering properties.