Male Infertility: Role of Cellular, Biochemical and Molecular Events

Abstract

Infertility is a unique category of human functional disability, where the fertility disturbances of one partner may only become evident through the other partner’s problem, while optimal reproductive function in one partner may compensate for impaired function in the other. It is estimated that approximately 15% of married couples are infertile. Male factor infertility contributes to about 50% manifested as quantitative abnormality (azoospermia, cryptozoospermia and oligozoospermia), or as qualitative abnormality (asthenospermia, teratozoospermia and necrospermia) or both. Investigation of apoptosis in spermatogonia, spermatocytes and spermatids in the testis has been done extensively and many apoptotic factors have been identified. Testicular apoptosis has been reported in human specimens, but its correlation with serum gonadotropins and testosterone levels is not clear. It is assumed that somatic cells can die in the apoptotic, the autophagic, or the necrotic way but the mechanisms involved in the sperm death are obscure and the biological significance of apoptosis in ejaculated sperm is yet to be elucidated. Thus the goal of this article is to identify and discuss common themes in mitochondrial function and the apoptotic pathway related to mammalian reproduction. Apart from this finding the correlation of apoptosis with serum gonadotropins and testosterone levels will also help in correlating the processes taking place in spermatozoa responsible for male infertility.