Probing the Origins of 1,800 MHz Radio Frequency Electromagnetic Radiation Induced Damage in Mouse Immortalized Germ Cells and Spermatozoa in vitro: RF-EMR Impairs Male Germline Cells

As the use of mobile phone devices is now highly prevalent, many studies have soughtto evaluate the effects of the radiofrequency-electromagnetic radiation (RF-EMR) onboth human health and biology. While several such studies have shown RF-EMR iscapable of inducing cellular stress, the physicobiological origin of this stress remainslargely unresolved. To explore the effect of RF-EMR on the male reproductive system, weexposed cultured mouse spermatogonial GC1 and spermatocyte GC2 cell lines, as wellas cauda epididymal spermatozoa to a waveguide generating continuous wave RF-EMR(1.8 GHz, 0.15 and 1.5 W/kg). This study demonstrated that a 4 h exposure is capable ofinducing the generation of mitochondrial reactive oxygen species (ROS) in populations ofGC1 (7 vs. 18%; p < 0.001) and GC2 cells (11.5 vs. 16 %; p < 0.01), identifying ComplexIII of the electron transport chain (ETC) as the potential source of electrons producingROS. Assessing the generation of ROS in the presence of an antioxidant, penicillamine,as well as measuring lipid peroxidation via 4-hydroxynonenal levels, indicated that theelevated incidence of ROS generation observed under our exposure conditions did notnecessarily induce an overt cellular oxidative stress response. However, exposure toRF-EMR at 0.15 W/kg for 3 h did induce significant DNA fragmentation in spermatozoa(that was no longer significant after 4 h), assessed by the alkaline comet assay (p < 0.05).Furthermore, this fragmentation was accompanied by an induction of oxidative DNAdamage in the form of 8-hydroxy-2′-deoxyguanosine, which was significant (p < 0.05)after spermatozoa were exposed to RF-EMR for 4 h. At this exposure time point, adecline in sperm motility (p < 0.05) was also observed. This study contributes newevidence toward elucidating a mechanism to account for the effects of RF-EMR onbiological systems, proposing Complex III of the mitochondrial ETC as the key targetof this radiation