Infertility is defined as the failure of a couple in reproductive ages to conceive despite having sexual intercourse regularly for at least 1 year without the use of contraceptive methods (Vayena, Rowe, & Griffin, 2002). Infertility affects 15% of couples of reproductive age (Wang et al., 2003). Male factor infertility has been detected in 30%-40%, and female factor infertility has been detected in 40%-50% of infertile couples. Pathologies involving both men and women are observed in 20%-25% of couples. In 15% of couples, no causes can be identified despite thorough diagnostic examinations. Spermatogenesis is a complex process regulated by endocrine, paracrine and juxtacrine regulatory signals that involve Sertoli, Leydig, peritubular and germ cells (Cheng, Wong, Yan, & Mruk, 2010). Normal reproductive function depends on the delicate balance between the androgen receptor (AR) and the classical oestrogen receptors (ERs). There is evidence that oestradiol has important effects on spermatogenesis and male fertility (O'Donnell, Robertson, Jones, & Simpson, 2001). Oestradiol has been considered to play a regulatory role in spermatogenesis events, including spermatogenesis, spermatogonial proliferation, meiosis, Sertoli cell function, spermiation and sperm transport (Cacciola, Chioccarelli, Fasano, Pierantoni, & Cobellis, 2013). Oestradiol manifests its effects by acting on three different types of ER in the testis. Of these receptors, ERα and ERβ are primarily involved in genomic and rapid signalling (Hess et al., 2011), and the recently discovered membrane-bound G protein-coupled oestrogen receptor (GPER) mostly mediates nongenomic effects (Rago,