Effects of estrogen on spermatogenic disorders induced by cyclophosphamide in mice

Abstract

Objectives: Cyclophosphamide, is used as an anticancer drug in chemotherapy. Cyclophosphamide is highly gonadotoxic drugs. On the other hand, there is growing evidence that estrogen by having receptors on hypothalamus plays a role in the regulation of testicular functions. The aim of the present study was to evaluate the effects of estrogen on spermatogenic disorders induced by cyclophosphamide in mice. Methods:Mice were randomly allocated to six groups: I: Control ,II: Sham(received Olive oil as solvent) ,III: Receiving cyclophosphamide 100mg/kg/week for 5 weeks. IV: Receiving cyclophosphamide as previous group and estrogen 50?g/kg/day for 10 days. V: Receiving cyclophosphamide as previous group then after two weeks from last injection, received estrogen 50?g/kg/day for 10 days.VI: Receiving Estrogen 50?g/kg/day for 10 days. Results: Number of spermatogenic and somatic cells of testis were decreased in cyclophosphamide receiving group. Germinal epithelial cells were destroyed extensivly in group that received cyclophosphamide and estrogen simultaneously. Germinal epithelial cells were destroyed moderately in group that received estrogen after cyclophosphamide however in this group the number of sertoli and leydig cells were increased in comparison to cyclophosphamide and cyclophosphamide+estrogen group. Estrogen alone had destructive effects on all types of cells. Conclusion: Cyclophosphamide and cyclophosphamide+estrogen destroys spermatogenesis. Receiving estrogen after cyclophosphamide treatment could be more appropriate because of increasing the number of sertoli and leydig cells and spermatogonia. However using estrogen as a protective agent after treatment with cyclophosphamide is not recommended.