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Oxidative Medicine and Cellular Longevity
Volume 2012 (2012), Article ID 929285, 15 pages
Review Article

The Hypoxic Testicle: Physiology and Pathophysiology

1Instituto de Química, Facultad de Ciencias, Pontificia Universidad Católica de Valparaíso, 2340000 Valparaíso, Chile
2Departamento de Ingeniería Química, Facultad de Ingeniería, Ciencias y Administración, Universidad de La Frontera, 4780000 Temuco, Chile
3Departamento de Fisiología, Facultad de Ciencias Biológicas, Pontifica Universidad Católica de Chile, 8320000 Santiago, Chile
4Centro de Investigaciones Biomédicas, Escuela de Medicina, Universidad de Valparaíso, 2340000 Valparaíso, Chile

Received 5 May 2012; Revised 7 August 2012; Accepted 9 August 2012

Academic Editor: Vincent Pialoux

Copyright © 2012 Juan G. Reyes et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mammalian spermatogenesis is a complex biological process occurring in the seminiferous tubules in the testis. This process represents a delicate balance between cell proliferation, differentiation, and apoptosis. In most mammals, the testicles are kept in the scrotum 2 to 7°C below body core temperature, and the spermatogenic process proceeds with a blood and oxygen supply that is fairly independent of changes in other vascular beds in the body. Despite this apparently well-controlled local environment, pathologies such as varicocele or testicular torsion and environmental exposure to low oxygen (hypoxia) can result in changes in blood flow, nutrients, and oxygen supply along with an increased local temperature that may induce adverse effects on Leydig cell function and spermatogenesis. These conditions may lead to male subfertility or infertility. Our literature analyses and our own results suggest that conditions such as germ cell apoptosis and DNA damage are common features in hypoxia and varicocele and testicular torsion. Furthermore, oxidative damage seems to be present in these conditions during the initiation stages of germ cell damage and apoptosis. Other mechanisms like membrane-bound metalloproteinases and phospholipase A2 activation could also be part of the pathophysiological consequences of testicular hypoxia.