Background. Several recent studies have shown that a brief ischaemia applied during the onset of reperfusion (postconditioning) is cardioprotective in different animal models. The potential application of postconditioning to organs different from the heart, i.e. kidney, is not available and is investigated in the present study. We also tested the hypothesis that mitochondria play a central role in renal protection during reperfusion. Methods. Wistar rats were subjected to left nephrectomy and 90-min right kidney occlusion. In controls, the blood flow was restored without intervention. In postconditioned rats, complete reperfusion was preceded by 3 min, 6 min and 12 min of reperfusion in a consecutive sequence, each separated by 5 min of reocclusion. Animals were studied for 48 h. Mitochondrial respiratory chain function, rate of hydroperoxide production and carbonyl proteins were measured at the end of postconditioning and 24 h and 48 h after reperfusion. Results. BUN and creatinine significantly decreased in the postconditioning group as compared to control rats. Mitochondrial respiratory function was significantly impaired in control rats, mainly at the level of Complex II. Postconditioning significantly reduced this mitochondria impairment. The rate of mitochondrial peroxide production was higher in the control group than in the protected group at the end of postconditioning reperfusion. Moreover, mitochondrial protein oxidation was significantly higher in control rats than in the postconditioning group at the end of reperfusion. Conclusions. In the present study, postconditioning reduced renal functional injury and reduces mitochondria respiratory chain impairment, mitochondria peroxide production and protein damage.
- Oxidative stress
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