Abstract
Summary Losses in motility and fertilizing ability of stored semen can at least in part be attributed to lipid peroxidation of the sperm plasma membrane. Physiologically, mitochondrial respiration is the main source of reactive oxygen species (ROS). In processed semen, ROS originate from contaminating leucocytes and from spermatozoa with residual cytoplasm. In addition, normal spermatozoa produce ROS as a result of their flagellar activity. At low concentrations, ROS have positive biological effects and regulate physiological sperm functions. Mammalian sperm cell membranes have a specific lipid composition with a high content of polyunsaturated fatty acids, making them particularly susceptible to damage by ROS. Peroxidation increases membrane permeability and decreases metabolic activity of sperm cells. To control the effects of ROS, semen contains antioxidants. Enzymatic antioxidants are glutathione peroxidase, superoxide dismutase and catalase. Antioxidants have been substituted in semen through the diet or by adding antioxidants to semen extender. However, as the loss of sperm motility during cooled-storage is not only an effect of plasma membrane dysfunction but also of mitochondrial membrane dysfunction, addition of antioxidants to semen during cooled-storage may have only limited effects.
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