In general, the ability of cells to tolerate low body temperatures is better than their ability to tolerate high body temperatures, and there is less resistance to body temperatures above the set-point temperature. In particular, an optimum testicular temperature, which is lower than the core body temperature, is crucial

Department of Urology, Yamaguchi University, Ube, Yamaguchi, Japan e-mail: [email protected]

A. Agarwal et al. (eds.), Studies on Men's Health and Fertility, Oxidative Stress 149

in Applied Basic Research and Clinical Practice, DOI 10.1007/978-1-61779-776-7_8, © Springer Science+Business Media, LLC 2012

for spermatogenesis. Normal testicular function is temperature-dependent, and in most mammals, the testes are maintained between 2 to 8°C below the core body temperature by the exteriorization of the testes in special hairless sacs called the scrotum [1, 2], In fact, slight increases in testicular temperature can disturb spermatogenesis and ultimately inhibit spermatogenesis. For example, temporal exposure of rodent testes to abdominal temperatures leads to marked disruption of spermatogenesis and infertility t 1, 3]. Moreover, ejaculates from men with scrotal temperatures above the normal range show increased incidence of abnormal and immature spermatozoa [4]. On the other hand, elevation of tes-ticular temperature has been suggested as a possible contraceptive treatment for men. Furthermore, elevation of testicular temperature impairs progressive sperm motility and viability, and sperm from heat-shocked testes results in a low in vitro fertilization rate [1]. Precoital testicular heating leads to a transient retardation in embryo growth and an increase in the rate of embryonic degeneration [1, 5-7], Taken together, these observations indicate that elevation of testicular temperature impairs not only spermatogenesis, but also sperm function and sperm DNA status. Temperatures lower than the normal temperature would lead to reduced metabolic rate and oxidative DNA damage in the testis because of active mitosis and meiosis of the germ cells.

Because of high cellular turnover, spermatogenesis per se requires extensive tissue restructuring in the seminiferous epithelium, resulting in the production of reactive oxygen species (ROS) and reactive nitrogen species, such as superoxide, hydroxyl, peroxyl, hydroperoxyl, nitric oxide, and nitrogen dioxide, which are produced by the peroxidation and oxidation of many cellular lipids, proteins, carbohydrates, and nucleic acids. Thus, germ cells are exposed constantly to thousands of free radicals and oxidative stress. Oxidative stress has been implicated in a variety of pathophysiological states, which cause male infertility [8]. Oxidative stress in heat-induced testicular injury is thought to be involved in clinical situations and may cause all testicular disorders. Research on heat-induced injury in the testes has a long history and is well studied compared with other organs, but the involvement of oxidative stress in heat-induced testicular injury has been a recent focus of research. In addition, many studies showed that ROS-scavenging mechanisms involving antioxidants in the testis play an important role in protecting germ cells against heat stress. Many studies have investigated oxidative stress in germ cells by using semen and ejaculated sperm; however, it should be mentioned that oxidative stress in semen is different from that in the testes. Difficulties in obtaining human testicular samples to examine gaseous molecules prevent the investigation of oxidative stress in the human testis. This chapter focuses on molecular events in the testis, mainly by using animal studies, and clinical situations caused by heat-induced testicular disorders, with special attention to oxidative stress. In addition, effects of oxidative stress on Sertoli and Leydig cells are discussed, because spermatogenesis is closely regulated by the cross-talk between germ and somatic cells.

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