Halil Ibrahim Tanriverdi1, Ufuk Şenel2, Fikret Gevrek3, Ali Akbaş4. 1. Pediatric Surgery, Manisa Celal Bayar University Medical School, Department of Pediatric Surgery, Manisa, Turkey. Electronic address: tanriverdi@cbu.edu.tr. 2. Pediatric Surgery, Gaziosmanpasa University Medical School, Department of Pediatric Surgery, Tokat, Turkey. Electronic address: ufuksenel@hotmail.com. 3. Histology and Embriology, Gaziosmanpasa University Medical School, Department of Histology and Embriology, Tokat, Turkey. Electronic address: fikretg05@hotmail.com. 4. Biochemistry, Balıkesir University Medical School, Department of Biochemistry, Balıkesir, Turkey. Electronic address: draliakbas@hotmail.com.
Abstract
INTRODUCTION: In testicular torsion, testicular blood flow is impaired, resulting in ischemic changes. Torsion must be corrected urgently with surgical treatment. Detorsioning and restoration of blood supply to the testis cause reperfusion injury. OBJECTIVE: In this experimental study, we aimed to investigate the effect of famotidine on ischemia-reperfusion injury in a rat model of testicular torsion. STUDY DESIGN: The rats were randomly divided into three groups; Group I (control, no torsion) (n = 8), Group II (torsion + detorsion) (n = 8), Group III (torsion + detorsion + famotidine) (n = 8). Levels of oxidative stress markers, such as malondialdehyde (MDA) and nitric oxide (NO), and antioxidants, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), were measured for biochemical analysis. Testicular tissues were assessed by Johnsen Scoring for spermatogenic evaluation. Tissues were also examined with TUNEL staining to determine the extent of apoptosis. RESULTS: Average MDA level was higher in Group II than Groups I and III. The difference was only significant between Group I and II (p = 0.03). Average NO level was significantly higher in Group II than Groups I and III (p = 0.03; p = 0.04; respectively). Conversely, average SOD level was lower in Group II than Groups I and III. The difference was only significant between Group II and III (p < 0.001). Average GSH-Px level was lower in Group II than Groups I and III, but the differences were not significant (p = 0.37; p = 0.35; respectively). The average Johnsen score in Group II was significantly lower than the scores in Groups I and III (p < 0.001; p < 0.001; respectively). The apoptotic index of Group II was significantly higher than those of Groups I and III (p < 0.001; p < 0.001; respectively). DISCUSSION: Famotidine prevented increases in oxidative stress markers and reductions of antioxidants during ischemia-reperfusion injury in our study. Spermatogenesis was less affected and DNA injury was reduced in rats treated with famotidine. The antioxidant characteristics of famotidine and its protective effects have been shown in our study. CONCLUSION: Famotidine may prevent oxidative tissue injury during ischemia-reperfusion.
INTRODUCTION: In testicular torsion, testicular blood flow is impaired, resulting in ischemic changes. Torsion must be corrected urgently with surgical treatment. Detorsioning and restoration of blood supply to the testis cause reperfusion injury. OBJECTIVE: In this experimental study, we aimed to investigate the effect of famotidine on ischemia-reperfusion injury in a rat model of testicular torsion. STUDY DESIGN: The rats were randomly divided into three groups; Group I (control, no torsion) (n = 8), Group II (torsion + detorsion) (n = 8), Group III (torsion + detorsion + famotidine) (n = 8). Levels of oxidative stress markers, such as malondialdehyde (MDA) and nitric oxide (NO), and antioxidants, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), were measured for biochemical analysis. Testicular tissues were assessed by Johnsen Scoring for spermatogenic evaluation. Tissues were also examined with TUNEL staining to determine the extent of apoptosis. RESULTS: Average MDA level was higher in Group II than Groups I and III. The difference was only significant between Group I and II (p = 0.03). Average NO level was significantly higher in Group II than Groups I and III (p = 0.03; p = 0.04; respectively). Conversely, average SOD level was lower in Group II than Groups I and III. The difference was only significant between Group II and III (p < 0.001). Average GSH-Px level was lower in Group II than Groups I and III, but the differences were not significant (p = 0.37; p = 0.35; respectively). The average Johnsen score in Group II was significantly lower than the scores in Groups I and III (p < 0.001; p < 0.001; respectively). The apoptotic index of Group II was significantly higher than those of Groups I and III (p < 0.001; p < 0.001; respectively). DISCUSSION: Famotidine prevented increases in oxidative stress markers and reductions of antioxidants during ischemia-reperfusion injury in our study. Spermatogenesis was less affected and DNA injury was reduced in rats treated with famotidine. The antioxidant characteristics of famotidine and its protective effects have been shown in our study. CONCLUSION:Famotidine may prevent oxidative tissue injury during ischemia-reperfusion.