The pathophysiology of testicular torsion-detorsion is an ischemia-reperfusion injury caused by overgeneration of reactive oxygen species (ROS). This study aimed to investigate the effect of rutin, a well-known antioxidant, on testicular ischemia-reperfusion injury.
Sixty male Sprague-Dawley rats were randomly divided into 3 groups, each containing 20 rats. Rats in the control group underwent a sham operation of the left testis. In the torsion-detorsion group, the left testis was rotated 720° for 2 hours. Rats in the treatment group received the same surgical procedure as the torsion-detorsion group, but rutin was administered intravenously at the time of detorsion. Bilateral orchiectomy was performed on half of the rats in each experimental group at 4 hours after detorsion for measurement of malondialdehyde, an indicator of intratesticular ROS content, and for evaluation of superoxide dismutase and catalase, which are endogenous antioxidant enzymes. Orchiectomy was performed on the remaining rats at 3 months after detorsion for analysis of testicular spermatogenesis.
Unilateral testicular torsion-detorsion caused a significant increase in malondialdehyde level and caused significant decreases in superoxide dismutase, catalase activities, and spermatogenesis in ipsilateral testes. The rats treated with rutin had a significant decrease in malondialdehyde level and had significant increases in superoxide dismutase, catalase activities, and spermatogenesis in ipsilateral testes, compared with torsion-detorsion group.
Rutin protects testes from ischemia-reperfusion injury. The protective effect of rutin may be caused by scavenging ROS by increasing superoxide dismutase and catalase activities.
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Accepted: September 20, 2010
Received in revised form: September 20, 2010
Received: August 23, 2010
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