The production of reactive oxygen species (ROS) is a normal physiological event in the male germ line. ROS are a double-edged sword, despite its role as key signaling molecules in physiological processes such as capacitation and hyperactivation, its overproduction which overwhelms the body’s antioxidant defenses is thought to affect male fertility and normal embryonic development. The excess generation of ROS in semen by exogenous and endogenous factors has been recognized as detrimental etiologies for male infertilities. Spermatozoa are vulnerable to ROS attack because they are rich in mitochondria, have abundance of substrates for free radical attack and their capacity to protect themselves from oxidative stress is limited. The cytotoxic aldehydes generated as a result of lipid peroxidation are known to form adduct with the mitochondrial protein involved in electron transport chain and stimulate generation of ROS in mitochondria. ROS and their metabolites can lead to oxidative DNA damage in mitochondria and nucleus that eventually culminates in DNA fragmentation. The presence for large amount of damaged DNA is a major characteristic of defective human spermatozoa, which affect the fertility and pregnancy outcome. Thus, as a comprehensive approach, treatment of oxidative stress should involve strategies to reduce stress-provoking conditions to help reverse sperm dysfunction.
Part of the book: Novel Prospects in Oxidative and Nitrosative Stress