Background:The aim of this study is to investigate effects of selenium and enlighten the possible mechanism of action in a rat transverse musculocutaneous flap model following ischemia-reperfusion injury.Materials and Methods:In this study, an experimental model, which mimicked free tissue transfer, was applied. Twenty-four male Wistar Albino rats were divided into a control group (N=12), and a selenium treated group (N=12). A superiorly based transverse rectus abdominis musculocutaneous (TRAM) flap was elevated and an ischemic insult for 4 hours was given. In selenium treated group (Group 2), sodium selenite (0.625mg/kg) was injected intraperitoneally (i.p), 2 hours before the induction of ischemia. Six rats from each group were sacrificed at 24 hours after the operation and malonyldialdehyde (MDA), nitric oxide (NO), and glutathione (GSH) levels were measured biochemically, whereas the intensity of neutrophil infiltration was evaluated. For the rest of the rats in Group 2, sodium selenite was injected at the same dose everyday to the postoperative 10th day, in which the remaining 6 rats from each group were sacrificed. On postoperative 10th day, flap viability was assessed along with the evaluation of intensity of neovascularization.Results:In Group 1, MDA levels were higher significantly (P<0.05) when compared with Group 2. No statistical difference, however, was found for NO (P>0.05), and GSH (P>0.05) levels among Group 1 and 2. Neutrophil infiltration was more intense in Group 1, when compared with Group 2 whereas neovascularization was more abundant in samples of Group 2. Group 2 shows higher average flap surface areas when compared with Group 1 (P<0.05).Discussion:The results of this study demonstrated the preventive effect of selenium against ischemia-reperfusion injury by reducing tissue necrosis in muscle flaps possibly by decreasing MDA, increasing neovascularization, and decreasing neutrophil infiltration, thus suppressing inflammation.