Review/Oorsig Volume 23, Issue 01 - Page 9

Volume 23 • Issue 01 • 2019 with a variety of antioxidants that serve to counterbalance the effect of oxidative stress. Antioxidants can be divided into enzymatic and non-enzymatic antioxidants. events. • • • • • • Enzymatic antioxidants The key enzymatic antioxidants of this defence system by which free radicals are removed include: Superoxidase dismutase (SOD), Glutathione peroxidase (GPX) Catalase. Superoxide dismutase (SOD) is an enzyme with a generalised presence in the body and is influenced by Cu, Zn and Mn. Glutathione peroxidase (GSH-Px) is believed to be the most important extracellular antioxidant enzyme in mammals and is Se dependent. Catalase is an antioxidant enzyme present in cytoplasm that acts as a catalyst for the conversion of hydrogen peroxide to oxygen and water. Non-enzymatic antioxidants. Non-enzymatic antioxidants are known as synthetic antioxidants or dietary supplements and are low-molecular weight compounds which include the following. Vitamin C (Ascorbic acid). A water soluble vitamin that provides intracellular and extracellular antioxidant protection. Vitamin E (α-Tocopherol). A lipid soluble vitamin and is in principal a membrane bound antioxidant in cells. β- Carotene. These are pigments found in plants and react with superoxide. Uric acid. An important antioxidant in bovine erythrocytes (red blood cells) and act as a free radical scavenger. Glutathione (GSH). Abundant in all cell compartments and is important for protection of cell membrane. Reactive oxygen species in the male reproductive system. Cellular generation of reactive oxygen species (ROS) has now been demonstrated in spermatozoa of various mammalian species, including the rat, mouse, rabbit, horse, bull and humans and can be either beneficial or detrimental to reproductive Reactive oxygen species are generated by sperm metabolism and are required for maturation, capacitation and acrosome reaction but they also modify cellular compounds. The mechanisms by which oxidative stress limits the functional competence of mammalian spermatozoa involve: The peroxidation of lipids, The induction of oxidative DNA damage, The formation of protein adducts. ROS production in these cells involves electron leakage from spermatozoa mitochondria and consequently spermatozoa lose their motility, DNA integrity and vitality. This pathway also influences the female tract’s immune response to sperm antigens and future fertility. Currently oxidative stress is believed to be an important cause of idiopathic male infertility since gametes are susceptible to OS. Defective sperm function is the most prevalent cause of male infertility and statistics from the United States indicate that up to 40% of infertile men have elevated levels of ROS in their seminal plasma. Spermatozoa are equipped with antioxidant defence mechanisms and are likely to quench ROS, thereby protecting gonadal cells and mature spermatozoa from oxidative damage. When uncontrolled production of ROS exceeds the antioxidant capacity of the seminal plasma it results in oxidative stress. Spermatozoa are unable to restore the damage induced by oxidative stress because they lack the necessary cytoplasmic-enzyme repair systems which makes spermatozoa unique in their susceptibility to ROS. This is due to the fact that their cell membranes are rich in polyunsaturated fatty acids (PUFA), rendering them highly susceptible to oxygen induced damage mediated by lipid peroxidation (LPO).This process causes axonal damage, decreased sperm viability and increased mid- piece sperm morphological defects, all of which contribute to decreased sperm motility. The effect of trace mineral supplementation on semen quality of bulls needs further investigation. 9