Effect of dexmedetomidine on testicular torsion/detorsion damage in rats

Background and Objective: We assessed the antioxidant activity of dexmedetomidine (DEX) during an ischemic period in a rat model of testicular torsion/detorsion (T/DT) by using biochemical and histopathological methods. Methods: Wistar Albino male rats weighing 250–300 g were divided into three groups: sham (group S, n = 7); torsion/detorsion (group T/DT, n = 7), and DEX treatment (group DEX, n = 7). In the T/DT group, right testes were rotated 720° for 1 h. Group S served for normal basal values. Rats in group T/DT were operated to make T/DT, this group served as a control group. Group DEX received intraperitoneal DEX 10 µg · kg–1 after the 30-min torsion period. For measurement of total antioxidant enzyme activities and malondialdehyde (MDA) levels, testes of 7 animals in each group were excised after 4 h of reperfusion. Germ cell apoptosis was evaluated using the apoptosis protease-activating factor 1 (APAF-1) antibody in all groups and also on the expressions of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) were assessed within the bilateral testes. Results: Mean MDA levels in group T/DT were significantly higher than in groups S and DEX (p < 0.05). There were also significant decreases in mean total antioxidant activities in group T/DT when compared to groups S and DEX (p < 0.05). These values were significantly higher in group DEX than group T/DT. Germ cell apoptosis, eNOS and iNOS levels were significantly higher in group T/DT when compared to groups S and DEX (p < 0.05). Conclusions: DEX treatment has potential biochemical and histopathological benefits by preventing ischemia/reperfusion-related cellular damage in an experimental testicular torsion model. Preference of DEX for anesthesia during the detorsion procedure may attenuate ischemia-reperfusion injury.