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ABSTRACT-We evaluated the effects of =-tocopherol (vitamin E) on the products of lipid peroxidation and serum creatinine levels in a rat model of renal ischemia-reperfusion. The animals were submitted to sham operation or renal ischemia-reperfusion, and they were pretreated with =-tocopherol or the vehicle saline. In four groups, we analyzed the lipid peroxidation products by measuring malondialdehyde and chemiluminescence levels. In the other three groups, we studied the serum creatinine levels after the procedures. In our study, the pretreatment with =-tocopherol reduced significantly the lipid peroxidation of renal cells and renal dysfunction induced by renal ischemia-reperfusion in rats.Keywords: =-Tocopherol, Renal ischemia-reperfusion, Lipid peroxidation Renal ischemia-reperfusion is a necessary procedure in circumstances such as surgical revascularization of renal arteries, surgical treatment of suprarenal aortic aneurysms, partial nephrectomies and renal transplantation. Oxygen free radicals (OFR) were shown to contribute to the cellular damage induced by ischemia-reperfusion, probably due to their lipidic oxidative characteristics, and several agents have been used to minimize the OFR action in renal ischemia-reperfusion (1).=-Tocopherol (vitamin E) is localized in the cell membranes and contributes to their stability and seems to protect the membrane lipids against oxidative damage (2).The purpose of these studies was to investigate the efficacy of = -tocopherol in the reduction of injury induced by OFR in a rat model of renal ischemia-reperfusion.Male Wistar rats weighing 250 to 330 g were randomly assigned to the experiments for analysis of the renal cell lipid peroxidation and measurement of serum creatinine levels. All experiments were approved by the local Committee for Animal Use and Care. The animals received general anesthesia with 50 mg/kg, i.p. of thiopental solution (Cristália, São Paulo, Brazil; 50 mg/ml). Renal ischemia-reperfusion was performed through a left flank incision (2 to 2.5 cm) followed by the dissection of the left renal pedicle so as to expose the renal vessels. Nontraumatic vascular clamps were used to stop blood flow. Reperfusion was established by removing the clamps. The abdominal wall (muscular layer and skin) was closed with 3.0 polypropylene and 4.0 mononylon sutures. The animals were randomly distributed into four groups: I) control group (n = 10): rats pretreated with 0.9% NaCl solution, 1 ml/kg, i.p., given 1 h before the sham-operation; II) ischemia group (n = 9): rats undergoing renal ischemia for 50 min; III) ischemia-reperfusion group (n = 10): rats undergoing renal ischemia for 50 min and reperfusion for 50 min; and IV) =-tocopherol group (n = 10): rats pretreated with =-tocopherol solution (Aldrich, Milwaukee, WI, USA; 30 mg/ ml), 30 mg / kg, i.p., 72, 48, 24, 6 and 1 h before ischemia for 50 min followed by reperfusion for 50 min.Immediately after the procedures, the renal tissue was excised to measure OFR's-induced lipid peroxidation of the renal cell membran...

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Background/Aims: Some studies have shown that postischemic hepatic dysfunction is mainly due to oxygen free radicals that are generated by xanthine oxidase. The present study was undertaken to determine the effect of allopurinol, an inhibitor of xanthine oxidase, on oxidative stress, liver injury and histologic alterations induced by hepatic ischemia-reperfusion in rats. Methods: One hundred and sixty Wistar rats were used and divided into three groups. Group 1: sham operation; group 2: 50 min of ischemia followed by 1 h of reperfusion, and group 3: pretreatment with allopurinol and 50 min of ischemia followed by 1 h of reperfusion. The effect of allopurinol was evaluated by plasma levels of alanine aminotransferase and aspartate aminotransferase, histopathologic studies, and lipid peroxidation measured by the thiobarbituric acid reactive substances method and chemiluminescence initiated by tert-butyl hydroperoxide technique. Results: Ischemia followed by reperfusion promoted an increase in lipid peroxidation of the hepatic cells when compared to the sham-operated group (p < 0.05). This increase was attenuated in the group treated with allopurinol (p < 0.05). Allopurinol also showed a protective effect on hepatocellular necrosis (p < 0.05), and the plasma levels of liver enzymes returned earlier to the normal range in rats pretreated with allopurinol in comparison to those that did not receive the drug (p < 0.05). Conclusions: Allopurinol exerted a protective effect on hepatic ischemia and reperfusion in rats. The administration of this drug prior to liver operations should be considered to be submitted to trials in humans.