Rapamycin protects testes against germ cell apoptosis and oxidative stress induced by testicular ischemia-reperfusion

Rapamycin is an immunosuppressant compound with a broad spectrum of pharmacological 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 720o 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