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 RESEARCH ARTICLE
Year : 2015  |  Volume : 47  |  Issue : 2  |  Page : 185-189

Protective effects of amifostine on ischemia-reperfusion injury of rat kidneys


1 Department of General Surgery, Antalya Training and Research Hospital, Antalya, Turkey
2 Department of General Surgery, Akdeniz University, School of Medicine, Antalya, Turkey

Correspondence Address:
Burhan Mayir
Department of General Surgery, Antalya Training and Research Hospital, Antalya
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0253-7613.153427

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Objectives: Amifostine is a drug which can eliminate free oxygen radicals that appear in the body after radiation or chemotherapeutic agent exposure. It is used to decrease the renal toxicity of cisplatin. The aim of this study was to determine the role of amifostine in warm ischemia kidney model for prevention of ischemia/reperfusion injury and also to find out the mechanism for prevention from ischemia/reperfusion injury if such an effect does exist. Materials and Methods: Adult female rats (n = 40) that used in our study were divided into three groups. Group 1: Control (n = 8), group 2: Ischemia-control (n = 16), group 3: Amifostine treated (n = 16). The effect of amifostine on ischemia/reperfusion injury investigated in rat kidneys. Results: At the 7 th day, blood urea nitrogen level was statistically significantly higher in ischemia-control group than all groups (P = 0.001) and mean serum creatinine levels were found to be the highest in ischemia-control group (P = 0.091). Mean malondialdehyde levels in left kidneys removed on the 7 th day were not significantly different (P = 0.105) at all three groups. Between ischemia-control group and amifostine group, there was a significant difference in reduced glutathione (GSH) levels (P = 0.001). In amifostine group, grade 4 necrosis was not detected neither on 7 th day nor day 0. Conclusion: Amifostine could decrease the degree and severity of necrosis after reperfusion. Amifostine could not prevent membrane lipid peroxidation caused by superoxide anion radicals in kidney but they could protect tissues from the harmful effects of ischemia/reperfusion injury by increasing the level of reduced GSH which is a well-known oxygen radical eliminator.






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