Conclusion

In recent years, experimental and clinical studies have suggested that the injured testis may result in damage to the contralateral testis after unilateral testicular torsion. The result of a I/R injury to the testis may be related to significant increase in germ cell apoptosis due to high testicular oxidative stress following the reperfusion. However, the specific mechanisms still need to be clarified. Impaired spermatogen-esis has been reported in animals and humans after testicular torsion. Biochemical, hormonal, immunological, histopathological, and vasculogenic studies have been performed, but the results are still controversial. To avoid testicular loss and eventual impaired fertility, prompt diagnosis and immediate surgery are the most important issues for the treatment of these patients.

Many antioxidants and free radical scavengers have been proposed in recent years for treatment of testicular torsion-induced subfertility or infertility, and a number of animal studies published to indicate their possible application. However, the molecular mechanism by which antioxidants control testicular torsion-induced male fertility has not yet been clearly identified. As a result, antioxidant therapy such as carnitine, melatonin, selenium, ibuprofen, and resveratrol may represent a new nonhormonal option within a broader therapeutic strategy. Antioxidant therapy reestablishes adequate oxidative balance in terms of the ratio of prooxidants to scavenger factors in men with ROS-mediated testicular torsion-induced infertility. Experimentally tested drugs or methods of preventing testicular damage caused by torsion still await clinical application. Identification of pharmacologic agents, administered as adjunctive therapy to surgical repair for rescuing the testis from I/R injury, is a clinically important goal. In brief, additional works are being performed in this area to further assess the late effects of testicular torsion and antioxidant therapy.

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