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In mammals, spermatogenesis begins with diploid stem cells that resemble other somatic cells; it ends with highly specialized motile haploid cells that are remarkably unique in appearance and function. Continuous production of spermatozoa throughout life requires that spermatogonia replenish themselves. Type B spermatogonia undergo mitosis to give rise to diploid primary spermatocytes. The spermatocytes then cross the blood-testis barrier formed by the Sertoli tight junctions to the adluminal compartment. Spermiogenesis refers to the acquisition by the germ cell of several organelles and accessory structures such as the acrosome and the flagellum. Testosterone and follicle-stimulating hormone (FSH) are the two major regulatory hormones of spermatogenesis. FSH binding to its receptor activates adenylate cyclase, and the resultant rise in cAMP triggers binding of cAMP response element modulator (CREM) to ACT (activator of CREM). The complex then acts as a molecular master-switch for a number of genes involved in spermatogenesis.
This chapter reviews the empiric therapies available today for male infertility and discusses their mode of action. It reviews published literature on outcomes available and analyzes the evidence for use and dosing recommendations. With the exception of low-dose vitamin supplementation and aromatase inhibitors, empiric therapy is seldom recommended in the treatment of the infertile male. Gonadotropin-releasing hormone (GnRH) stimulates the synthesis and release of the gonadotropic hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), in the anterior pituitary. Treatment of hypogonadotropic hypogonadism with exogenous gonadotropins or GnRH has produced good results compared with treatment of other male infertility problems. Exogenous testosterone therapy can produce azoospermia or severe oligospermia through the inhibition of gonadotropin secretion. Glutathione therapy has been used in various pathologic conditions in which reactive oxygen species are thought to play a pathogenic role. Administration of high-dose antioxidants has a potential beneficial effect on male fertility.
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