%0 Journal Article
%T The Enzymatic Antioxidant System of Human Spermatozoa
%A Cristian O¡¯Flaherty
%J Advances in Andrology
%D 2014
%R 10.1155/2014/626374
%X The ejaculated spermatozoon, as an aerobic cell, must fight against toxic levels of reactive oxygen species (ROS) generated by its own metabolism but also by other sources such as abnormal spermatozoa, chemicals and toxicants, or the presence of leukocytes in semen. Mammalian spermatozoa are extremely sensitive to oxidative stress, a condition occurring when there is a net increase in ROS levels within the cell. Opportunely, this specialized cell has a battery of antioxidant enzymes (superoxide dismutase, peroxiredoxins, thioredoxins, thioredoxins reductases, and glutathione s-transferases) working in concert to assure normal sperm function. Any impairment of the antioxidant enzymatic activities will promote severe oxidative damage which is observed as plasma membrane lipid peroxidation, oxidation of structural proteins and enzymes, and oxidation of DNA bases that lead to abnormal sperm function. Altogether, these damages occurring in spermatozoa are associated with male infertility. The present review contains a description of the enzymatic antioxidant system of the human spermatozoon and a reevaluation of the role of its different components and highlights the necessity of sufficient supply of reducing agents (NADPH and reduced glutathione) to guarantee normal sperm function. 1. Introduction Mammalian and particularly human spermatozoa are sensitive to high levels of reactive oxygen species (ROS) [1, 2]. In the 40s, this toxic effect was first observed independently by different investigators: McLeod working with human and Tosic and Walton working with bull sperm samples; they found that the spermatozoon is very sensitive to high concentrations of hydrogen peroxide (H2O2) [3¨C5]. These pioneer works opened a new era of research in the biology of reproduction field to understand the mechanisms and players affected by toxic levels of ROS of sperm physiology. The oxidative stress is produced by a net increase of ROS levels because of an increase of their production and/or a decrease of antioxidant defences [6, 7]. It generates substantial damage to all components of the sperm cell; thus, significant levels of lipid peroxidation, protein, and DNA oxidation are seen in this situation [7, 8] and are often associated with infertility [9¨C12]. This damage is translated to changes in the plasma membrane fluidity, inactivation of key enzymes, and damage of the paternal DNA leading to impairment of sperm motility, mutations in the genomic message, and a variety of reproductive outcomes including, fertilization and embryo development failure, miscarriages, and
%U http://www.hindawi.com/journals/aandrol/2014/626374/