Hypoxic damage in the contralateral testis after unilateral testicular torsion in a rat model: Hemodynamic change and expressions of hypoxia inducible factor-1 α, VEGF and apoptosis in the contralateral testis

Purpose: The present study aimed to evaluate the hypoxic damage in the contralateral testis after unilateral testicular torsion in a rat model, using hemodynamic change, the expression of hypoxia inducible factor-1 α (HIF-1α) and apoptosis. Materials and methods: Thirty-five male albino Sprague-Dawley rats were randomly divided into 7 groups: 0 and 6 hours after sham operations, 6, 12 and 24 hours, and 3 and 7 days after the unilateral testicular torsion. Torsion was created by rotating the left testis 720 degrees, in a clockwise direction, which was maintained by fixing the testis to the scrotum with a silk suture. The testicular blood flow of the contralateral testis was measured by laser flowmetry, both before and after the testicular torsion. After bilateral orchiectomies had been performed in each group, the expressions of HIF-1α and vascular endothelial growth factor (VEGF), as well as apoptosis were determined by immunohistochemical staining and Western blot analysis. Results: The blood flow of the contralateral testis after the unilateral testicular torsion significantly decreased compared with that of the sham group (p<0.05). In the immunohistochemical staining, the expression of HIF-1α protein increased in the testicular torsion group compared to that of the sham group, and was markedly apparent 12 hours after the testicular torsion. The apoptotic cell index was also significantly higher in the testicular torsion group than in the sham group (p<0.05). In the Western blot study, the HIF-1α and VEGF expressions were increased in the testicular torsion group compared to those in the sham group 6 hours after the testicular torsion. Conclusions: This study suggests that the decreased testicular blood flow of the contralateral testis during ipsilateral testicular torsion induces HIF-1 α, resulting in apoptosis of germ cells.