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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.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 (0.625 mg/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.In Group 1, MDA levels were higher significantly (P0.05) when compared with Group 2. No statistical difference, however, was found for NO (P0.05), and GSH (P0.05) 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 (P0.05).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.

Ototoxicity is a common side effect of cisplatin chemotherapy. The aim of this study was to investigate the potential protective effect of chrysin against cisplatin-induced ototoxicity. Thirty-four adult female Wistar albino rats were separated into four groups: a cisplatin group (Group A), with cisplatin administered to ten rats once daily for three consecutive days at doses of 8 mg/kg body weight intraperitoneally (i.p.); a cisplatin plus chrysin group (Group B), with 8 mg/kg of cisplatin administered i.p. daily to ten rats for three consecutive days and 25 mg/kg of chrysin administered via oral gavage in a corn oil for 5 days: a chrysin group (Group C), with 25 mg/kg of chrysin administered via oral gavage in corn oil for 5 days to seven rats; and a control group (Group D), with 5 ml/kg of corn oil administered to seven rats via oral gavage for 5 days. Distortion product otoacoustic emission measurements were performed in the same ear of the rats under general anesthesia at baseline and on the first and fifth days after drug administration. No significant differences were noted between the measurements either in the chrysin group or in the control group. In the cisplatin group, there was a significant worsening of hearing compared to baseline and the measurements on the fifth day at all frequencies. In the statistical analysis, a statistically significant difference was observed at 5039, 6351, 8003, and 10078 Hz frequencies between the measurements on the first and fifth days. In the cisplatin plus chrysin group, there were statistically significant differences at frequencies of 2,003 and 5,039 Hz between the measurements at baseline and on the fifth day, at 3,175 and 5,039 Hz between the measurements on the first and fifth days, and at 8,003 and 100,078 Hz between the measurements at baseline and on the first day. According to these results, this study demonstrates that cisplatin-related ototoxicity can be prevented in rats by the administration of chrysin.