Involvement of reactive oxygen species and TATA box-binding protein-related factor 2 in testicular torsion/detorsion-induced injury.

OBJECTIVE:To investigate whether overproduction of reactive oxygen species after testicular torsion-detorsion injures testicular spermatogenesis by regulating expression of TATA box-binding protein-related factor 2 (TRF2), which is an essential transcription factor for spermatogenesis. Testicular torsion-detorsion causes overproduction of reactive oxygen species, which contributes to testicular injury and regulates many genes whose expression affects cell cycle regulation, cell proliferation, and apoptosis. MATERIALS AND METHODS:A total of 60 adult male Sprague-Dawley rats were divided into 3 groups of 20 rats each. The control group underwent a sham operation of the left testicle. The torsion-detorsion group received 1 hour of left testicular torsion. The scavenging reactive oxygen species group underwent the same surgical operation as the torsion-detorsion group, but superoxide dismutase and catalase, 2 well-known reactive oxygen species scavengers, were given intravenously at detorsion. The testicles were harvested 4 hours or 3 months after detorsion to measure the malondialdehyde level (a marker of reactive oxygen species), TRF2 expression, and spermatogenesis. RESULTS:Unilateral testicular torsion-detorsion significantly increased the malondialdehyde level and reduced TRF2 expression and spermatogenesis in ipsilateral testicles, suggesting that overgeneration of reactive oxygen species after testicular torsion-detorsion might downregulate TRF2 expression, leading to spermatogenic damage. In contrast, administration of superoxide dismutase and catalase significantly decreased the malondialdehyde level and increased TRF2 expression and spermatogenesis in ipsilateral testicles. These results supported the above suggestion. CONCLUSION:These findings have indicated that overproduction of reactive oxygen species after testicular torsion-detorsion can damage testicular spermatogenesis by downregulation of TRF2 expression.

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