Peroxidación lipídica y antioxidantes en la preservación de semen. Una revisión

In aerobic organisms oxygen is essential for life, but it can be toxic when favorable situations are presented in which an exaggerated production of reactive oxygen species (ROS): superoxide anion (O ₂) and hydroxyl (OH), and due to the generation of hydrogen peroxide (H ₂O ₂), a ROS that can be a precursor of free radicals. ROS contribute to the molecular and structural damage that is present in a series of ailments where the antioxidant capacity (antioxidants and enzymes) of the organism is surpassed and is therefore unable to inactivate them, giving rise to the process called oxidative stress. The oxidative damage in the cell membrane is induced by the free radicals that lead to lipoperoxidation. The freezing and unfreezing process of the semen reduces the percentage of live sperm cells, thus affecting their mobility and viability, and therefore the gamete's fertility, a phenomenon that is attributed to diverse factors, including temperature changes and ROS effects. During the metabolism of the spermatozoa, the mitochondria generate, unavoidably, ROS that are inactivated by the antioxidative mechanisms. To counteract the ROS effects generated by non-physiologic mechanisms or their excess, a variety of antioxidants has been used, seeking to annul or to minimize the effects. The object of this review is to identify the causes of damage to the spermatic cells during semen preservation and the antioxidative defense systems, both enzymatic and non-enzymatic.