Relative impact of oxidative stress on male reproductive function

Impairment of normal spermatogenesis and sperm function are the most common causes of male factor infertility. Abnormal sperm function is difficult to evaluate and treat. There is a lack of understanding of the factors contri buting to normal and abnormal sperm function leading to infertility. Many r ecent studies indicate that oxygen-derived free radicals induce damage to s permatozoa. The excessive generation of these reactive oxygen species (supe roxide, hydroxyl, nitric bride, peroxide, peroxynitrile) by immature and ab normal spermatozoa and by contaminating leukocytes associated with genitour inary tract inflammation have been identified with idiopathic male infertil ity. Mammalian spermatozoa membranes are rich in polyunsaturated fatty acid s. This makes them very susceptible to oxygen-induced damage, which is medi ated by lipid peroxidation. In a normal situation, the antioxidant mechanis ms present in the reproductive tissues and their secretions ate likely to q uench these reactive oxygen species (ROS) and protect against oxidative dam age to gonadal cells and mature spermatozoa. During chronic disease states, aging, toxin exposure, or genitourinary infection/inflammation, these cell ular antioxidant mechanisms downplay and create a situation called oxidativ e stress. Thus, a balance between ROS generation and antioxidant capacity p lays a critical role in the pathophysiology of disease state. Recent effort s towards the development of new reliable assays to evaluate this oxidative stress status have resulted in the establishment of ROS-TAC score. Such as sessment of oxidative stress status (OSS) may help in designing newer modes of male factor infertility treatment by suitable antioxidants.