Mammalian semen is a physiological fluid composed of a cellular fraction (spermatozoa), and a liquid fraction (seminal plasma). Once delivered to the female genital tract, spermatozoa should be able to capacitate; a process which involves a plethora of biochemical and physiological changes required to fertilize the oocyte. Sperm production (spermatogenesis) occurs in the testes, whereby pluripotent spermatogonia differentiate to form the most morphologically specialized cells in the body. Further maturation of spermatozoa occurs in the epididymis, where they are stored prior to ejaculation. During this whole process, spermatozoa are exposed to different environments and cellular processes which may expose them to substantial levels of oxidative stress. To avoid damage associated with the unchecked production of reactive oxygen species (ROS), both spermatozoa, and the parts of the male genital tract in which they reside, are furnished with a suite of antioxidant molecules which are able to provide protection to these cells, thereby increasing their chance of being able to fertilize the oocyte and deliver an intact paternal genome to the future offspring. However, there are a host of reasons why these antioxidant systems may fail, including nutritional deficiencies, genetics, and disease states, and in these situations, a reduction or abolition of fertilizing capacity may result. This review paper focuses on the endogenous antioxidant defences available to spermatozoa during spermatogenesis and sperm maturation, the site of their production and their physiological role. Furthermore, we revised the causes and effects of antioxidant deficiencies (congenital or acquired during the animal's adulthood) on reproductive function in different animal species.
Keywords: Antioxidant; Oxidative stress; Reactive oxygen species; Reproduction; Sperm.
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