*3.1. Physical Factors*

One of the contemporary issues of the modern lifestyle is excess heating of testes. In scrotal animals such as our own, the testicular environment has evolved to operate optimally at temperatures that generally lie at least 1–2 ◦C below that of core body temperature (reviewed in [48]). Accordingly, the spermatogenic process can be adversely impacted by scrotal hyperthermia as occurs in certain professions such as those that involve extended periods of seated activity (e.g., at a desk or in a vehicle) or those that involve direct exposure to high ambient temperatures (e.g., steel fabrication and welding). The occupational practice of using a laptop computer in such a way that it covers the testes can also cause localized heat stress, as does the wearing of tight clothing and in particular, underwear. Through mechanisms described in the previous section, the heat-stressed testes have been shown to produce excessive ROS, which is linked to the impairment of sperm function [49,50]. It should be noted that alternative lifestyle habits such as frequent sauna or warm bath exposures also represent potential sources of heat stress that may impact on male infertility [51–53]. In support of this conclusion, a recent study by Houston et al. [54] demonstrated that the exposure of mice to elevated ambient temperature led to increased sperm mitochondrial ROS generation and OS-induced molecular changes during germ cell development.

Similarly, increasing attention has been focused on the potential impact of non-ionizing radiation, such as the electromagnetic energy (EME) emitted by mobile technologies and other forms of microwave equipment, on the male germ line [55]. In this context, the human body has the potential to behave in a manner analogous to that of an antenna that receives EME [56]. The exposure of human tissues to EME can have various biological e ffects including localized elevation of the temperature in the a ffected tissue, including the testes [56]. EME can also alter cellular membrane potential and impact molecular bonding, with the polar side chains of amino acids being particularly a ffected by EME exposure [57]. Such changes not only have the potential to influence protein structure, and hence interfere with enzymatic activity, but can also perturb the transmembrane transport of ions [56,57]. As an extension of these findings, multiple studies have now demonstrated that supraphysiological levels of EME can negatively a ffect mitochondrial membrane characteristics and/or overall functioning [58–60]. Indeed, the exposure of isolated cells to EME can lead to increased activation of mitochondrial function and an attendant elevation of ROS production associated with complexes I and III of ETC, independent of changes in mitochondrial membrane potential [56,58]. In model cells such as those of the human amniotic epithelial lineage, magnetic fields can induce mitochondrial permeability transition and cytochrome-c release together with increased intracellular ROS generation, via a pathway that is dependent on glycogen synthase kinase-3β [58]. As proof of concept, it has also been shown that human spermatozoa exposed to EME at frequencies designed to simulate that emitted by mobile phones experience reduced motility and vitality; defects that were associated with increased mitochondrial ROS production and numerous molecular alterations that are synonymous with OS [59].
