Caspases and Spermatogenesis

During spermatogenesis, the number and quality of germ cells are balanced via apoptosis. In adults, close to 75% of spermatogonia and to lesser extent spermatocyte and spermatid are lost [17, 18]. It has been shown that germ cell apoptosis at the cellular level is controlled by endocrinal and local factors and at the intracellular level by p53 and caspases [19, 20]. Although procaspase-3, -6, and -7 and also the IAP caspase inhibitor have been found in normal histology of testis, activated forms of caspase-3, -6, and -7 were not found in normal testis using western blotting or immunohistochemistry methods. Procaspase-3 expression has been shown in testes with normal spermatogenesis and also in testis with sperm maturation arrest or ser-toli cell only (SCO). Kim et al. [21] found a diffuse signal for activated caspase-3 in sertoli and germ cell and also leydig cell in testes with sperm maturation arrest; however, the expression of activated caspase-3 has never been seen in testes with normal spermatogenesis [22]. Research suggests that spermatogenic arrest could be related to increased apoptotic rate in testes and increase of activated caspase-3 [22]. In contrast, varicocele patient [23] and hypospermatogenesis and SCO are associated with low level of apoptosis [24]. In the testes, the expression of CD95 and its receptor, which have been introduced as key regulators for germ cell apoptosis [25, 26], is localized to the germ and Sertoli cells [27]. The downstream factors of CD95 activation include various caspases, among which the caspase-8 has the most significant role [28].

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