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Updated: Feb 19, 2026
Germ Cell Transplantation and Testis Tissue Xenografting in Mice
Published on: February 6, 2012
Rapamycin protects testes against germ cell apoptosis and oxidative stress induced by testicular ischemia-reperfusion
Morteza Ghasemnejad-Berenji1,2,3, Mahmoud Ghazi-Khansari1, Iraj Yazdani1,2
1Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Objectives:
Rapamycin is an immunosuppressant compound with a broad spectrum of pharmaco-logical activities. In recent years, it has been used successfully to decrease ischemia-reperfusion injury in several organ systems. The purpose of the present study was to examine the effect of rapamycin on testicular ischemia-reperfusion injury.
Materials And Methods:
Seventy-two adult male Wistar rats were divided into six groups: control (group1), sham-operated (Group2), T/D + DMSO as vehicle group (group3), and groups 4-6; respectively received 0.5, 1, and 1.5 mgkg-1 of rapamycin, IP 30 min before detorsion. Ischemia was achieved by twisting the right testis 720° clockwise for 1 hr. The right testis of 6 animals from each group were excised 4 hr after detorsion for the measurement of lipid peroxidation, caspase-3, and antioxidant enzyme activities. Histopathological changes and germ cell apoptosis were determined by measuring mean of seminiferous tubules diameters (MSTD) and TUNEL test in right testis of 6 animals per group, 24 hr after detorsion.
Results:
Testicular T/D caused increases in the apoptosis, malondialdehyde (MDA), and caspase-3 levels and decreases in the superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in ipsilateral testis (P<0.001). The rats treated with rapamycin had significant decreases in the MDA and caspase-3 levels and significant increases in the SOD, CAT and GPx activities in ipsilateral testis compared with the T/D group (P<0.001); germ cell apoptosis was decreased, and MSTD was improved.
Conclusion:
Rapamycin administration during testicular torsion decreased ischemia/reperfusion (I/R) cellular damage.
Insights
Rapamycin treatment significantly reduced testicular damage caused by ischemia-reperfusion injury in rats. This immunosuppressant improved tissue health and decreased cell death, offering potential therapeutic benefits.
Area of Science:
- Urology
- Pharmacology
- Cell Biology
Background:
- Ischemia-reperfusion (I/R) injury is a significant concern in testicular torsion.
- Rapamycin, an immunosuppressant, has shown promise in mitigating I/R injury in other organs.
Purpose of the Study:
- To investigate the efficacy of rapamycin in preventing testicular ischemia-reperfusion injury in a rat model.
Main Methods:
- Adult male Wistar rats underwent testicular torsion/detorsion (T/D).
- Rats were treated with varying doses of rapamycin or vehicle prior to detorsion.
- Biochemical markers (MDA, caspase-3, antioxidant enzymes), histopathology (MSTD), and apoptosis (TUNEL) were assessed.
Main Results:
- Testicular T/D significantly increased apoptosis, MDA, and caspase-3, while decreasing antioxidant enzyme activity.
- Rapamycin treatment dose-dependently reduced MDA and caspase-3 levels.
- Rapamycin administration increased superoxide dismutase, catalase, and glutathione peroxidase activities, decreased germ cell apoptosis, and improved mean seminiferous tubule diameter.
Conclusions:
- Rapamycin effectively mitigates testicular ischemia-reperfusion injury.
- The findings suggest rapamycin's potential as a therapeutic agent for testicular torsion.
