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Title: The biochemical effects of ischemia-reperfusion injury in the ipsilateral and contralateral testes of rats and the protective role of melatonin. Author: Parlaktas BS, Atilgan D, Ozyurt H, Gencten Y, Akbas A, Erdemir F, Uluocak N. Journal: Asian J Androl; 2014; 16(2):314-8. PubMed ID: 24407181. Abstract: Testicular torsion (TT) is a serious urologic emergency that is observed in adolescent males and that can lead to infertility if left untreated. The ischemia-reperfusion (I/R) injury due to TT has been implicated in the pathogenesis of testicular damage. We investigated the effects of melatonin on oxidative damage in the ipsilateral and contralateral testes of rats induced by unilateral TT. A total of 21 prepubertal male Wistar albino rats were divided into three groups, each consisting of seven rats. In Group 1 (SHAM group): a sham operation to the left testis and bilateral orchiectomy were performed. In Group 2 (I/R group): I/R injury was created by rotating the left testis 720° in a clockwise direction for 2 h and detorsing the testis after 2 h. Group 3 (I/R + MEL group): rats were subjected to I/R injury and one-shot melatonin injection (50 mg kg?1, intraperitoneal (i.p.)). The testes of the rats were excised bilaterally in all groups. The testicular tissue activities of antioxidant catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase enzymes (GSH-Px), and the tissue levels of malondialdehyde (MDA), protein carbonyl (PC) and nitric oxide (NO) were determined. Administration of melatonin caused a significant decrease in lipid peroxidation and enzyme activities in the ipsilateral testis when compared with the control group (P < 0.05). All of the changes in the enzyme activities of the contralateral testis were insignificant (P > 0.05). MDA levels were signifi cantly altered in the contralateral testis (P = 0.009). Melatonin administration decreased the deleterious effects of I/R injury in the ipsilateral torted testes of the rats. The contralateral testes were slightly affected by unilateral TT.[Abstract] [Full Text] [Related] [New Search]