Stress and Cell Death in Testicular CellsJuárez-Rojas, Lizbeth, Casillas Fahiel and Retana-Márquez Socorro*
Department of Biology of Reproduction, Autonomous University Metropolitan Iztapalapa, San Rafael Atlixco 186, Mexico City, México
- *Corresponding Author:
- Retana-Márquez Socorro
Department of Biology of Reproduction
Autonomous University Metropolitan Iztapalapa
San Rafael Atlixco, Mexico City, México
Fax: 52 5558044930
E-mail: [email protected]
Received date: May 19, 2017; Accepted date: Jun 05, 2017; Published date: Jun 10, 2017
Citation: Rojas J, Lizbeth, Fahiel C, Socorro RM (2017) Stress and Cell Death in Testicular Cells. Andrology (Los Angel) 6:183. doi: 10.4172/2167-0250.1000183
Copyright: © 2017 Rojas J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The success of male reproduction requires the production of a large number of spermatozoa by a unique process known as spermatogenesis. Spermatogenesis is carried out in close association with the Sertoli cells, the only somatic cells of the seminiferous epithelium which are responsible for providing structural, nutritional and endocrine support to the developing germ cells. The seminiferous epithelium of the testes is a rapid proliferation tissue, where the germinal cells, through a large number of mitotic and meiotic divisions prior to their differentiation culminate with the structural and functional formation of spermatozoa. The number of germ cells that Sertoli cells can sustain is maintained by apoptosis, which fulfills the elimination of germ cells with genetic errors, damage to DNA or excess cell production. Apoptosis can also be activated by external factors such as stress, causing alterations in spermatogenesis and testicular involution, which compromises fertility. However, death in testicular cells is not attributed only to apoptosis, as cells use different mechanisms to activate their self-elimination, such as anoikis and autophagy. All of these mechanisms are discussed.