Effect of unilateral testicular torsion on contralateral testis in a rat model
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In brief
In brief
Rat model study demonstrates unilateral testicular torsion causes contralateral testicular damage through early ischemia-reperfusion injury and late autoimmune response, resulting in impaired spermatogenesis. Cyclosporine and L-NMMA treatments showed protective effects on contralateral testis function and sperm parameters.
Written by the GCMD Library team from the article.
Abstract
Objective
The aim of this study was to investigate the function of the contralateral testis after unilateral testicular torsion (UTT) and its possible mechanism.
Methods
56 rats were randomly divided into four groups: Group A: Sham operation, Group B: Testicular torsion (TT)+normal saline (NS), Group C: Testicular torsion (TT)+cyclosporine, Group D: Testicular torsion (TT)+NG-Monomethyl-l-arginine (l-NMMA). The right testes were removed 1 week and 8 weeks after surgery, respectively. Biochemistry and histopathologic evaluations were used to evaluate the germ cell damage.
Results
Compared with Group A, the levels of malondialchehyche (MDA) and nitric oxide (NO)/nitricoxide synthase (NOS) were increased remarkably in Group B. Significant differences were shown between histopathological damages and density and motility of sperm in two groups. Compared with Group B, the levels of MDA and NO/NOS in Group D decreased significantly while mean seminiferous tubule diameter (MSTD) and mean testicular biopsy scoring (MTBS) maintained in a better condition. The levels of major histocompatibility complex (MHC) peptide-tetramer complex in Group C and Group D decreased significantly than Group B, while sperm density and motility were significantly higher than Group B. It was also known that the histopathological damages in Group C and Group D were less than those in Group B in the 8 weeks after operation.
Conclusion
UTT can cause impairment of contralateral testicular function and decrease of spermatogenic function. The mechanism may be related to ischemia–reperfusion (IR) in early stage and autoimmune response in late stage.