Objective- Cryptorchidism, common birth defect of the male genital tract, is one of the causes of fertility problems. The elevation of tissue temperature following of cryptorchidism could induce oxidative stress which influences the cellular and tissue degeneration. Amlodipine is a third-generation of calcium channel blockers which has antioxidant activity. The aim of this study was to evaluate the protective effects of amlodipine on testicular tissue alterations in an animal model of cryptorchidism.
Design- Experimental study
Animals- Thirty adult male Sprague-Dawley rats weighing 200-220g
Procedure- Experimental cryptorchidism was induced in adult rats. Amlodipine (10 mg/kg b.w.) was administrated orally for two and four consecutive weeks. The experimental groups consisted of non-treated cryptorchidism (n=10) and treated cryptorchidism (n=10) groups. Testicular tissue samples were collected on days 14 and 28 following of cryptorchidism form non-treated and treated groups. Histopathological and morphometrical studies with the evaluation of microscopic indices of spermatogenesis were prepared on tissue samples.
Results- Tubular atrophy with germinal epithelium disarrangement was observed in cryptorchidism groups. These changes were reduced dose-dependently in treated animals. The mean of Sertoli cells was reduced significantly (p=0.025) in four weeks non-treated and the mean of germ cells lineage was reduced significantly (p<0.0001) in four weeks non-treated and two weeks treated cryptorchidism groups compared to the control group. Similarly, all microscopic indices of spermatogenesis were reduced following the induction of cryptorchidism. These alterations were reduced time-dependently in amlodipine treated groups.
Conclusion and clinical relevance- The results of this study revealed that the administration of amlodipine as an antioxidant agent, time-dependently could be effective on the reduction of cellular and tissue damages of testicular tissue induced by cryptorchidism. It seems some parts of these protective effects may be done through its activity as calcium blocker which declines apoptotic processes by reduction of cytoplasmic calcium levels.