Beneficial effect of N-acetyl-cysteine on renal injury triggered by ischemia and reperfusion.
Reactive oxygen species are critical mediators of the early phase of ischemic (IR) injury. The contribution of antioxidants, such as N-acetyl-cysteine (NAC), in ameliorating the parenchymal lesions, inflammatory parameters, and functional variables in renal IR is still controversial. We studied the effect of NAC administration on renal injury induced by IR. Mice were subjected to renal pedicle occlusion and subsequent reperfusion for 24 or 120 hours. NAC was administered prior to surgery at two concentrations (40 or 300 mg/kg, i.p.). Renal function and acute tubular necrosis were assessed, as well as immune phenotyping of infiltrating cells, by flow cytometry. At 40 mg/dL of NAC, we did not observe any significant improvement in renal function (1.85 +/- 0.43 md/dL, P = .367) or tissue architecture (% of ATN: 2.51 +/- 0.27 mm, P = .852) compared to the controls (1.87 +/- 0.43 mg/dL and 3.12 +/- 0.34 mm, respectively). However, animals that received 300 mg/dL of NAC showed lower serum creatinine values (24 hours: 1.25 +/- 0.54 mg/dL) compared to controls (P = .009) and less extensive acute tubular necrosis (1.54 +/- 0.12 vs, P < .05). Treatment with 300 mg/dL of NAC decreased renal dendritic cell infiltration. The protective effect of NAC was better observed at high concentrations and early times.