Abstract

As the use of mobile phone devices is now highly prevalent, many studies have sought to evaluate the effects of the radiofrequency-electromagnetic radiation (RF-EMR) on both human health and biology. While several such studies have shown RF-EMR is capable of inducing cellular stress, the physicobiological origin of this stress remains largely unresolved. To explore the effect of RF-EMR on the male reproductive system, we exposed cultured mouse spermatogonial GC1 and spermatocyte GC2 cell lines, as well as 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 of inducing the generation of mitochondrial reactive oxygen species (ROS) in populations of GC1 (7 vs. 18%; p < 0.001) and GC2 cells (11.5 vs. 16 %; p < 0.01), identifying Complex III of the electron transport chain (ETC) as the potential source of electrons producing ROS. Assessing the generation of ROS in the presence of an antioxidant, penicillamine, as well as measuring lipid peroxidation via 4-hydroxynonenal levels, indicated that the elevated incidence of ROS generation observed under our exposure conditions did not necessarily induce an overt cellular oxidative stress response. However, exposure to RF-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 DNA damage 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, a decline in sperm motility (p < 0.05) was also observed. This study contributes new evidence toward elucidating a mechanism to account for the effects of RF-EMR on biological systems, proposing Complex III of the mitochondrial ETC as the key target of this radiation.

Highlights

  • Mobile phone usage is becoming increasingly popular worldwide and our exposure to the radiofrequencyelectromagnetic radiation (RF-EMR) emitted by these devices is unprecedented [1,2,3]

  • Given that the mitochondria account for a majority of reactive oxygen species (ROS) production within the mature spermatozoon [34, 38] and the observed increase in mitochondrial ROS generation following germ cell exposure to RF-EMR (Figures 1A,B), we investigated the effects of treating GC1/GC2 germ cell lines with a combination of RF-EMR and inhibitors that selectively target either Complex I or III of the electron transport chain (ETC) (Figure 2)

  • In this study we have explored the effects of RF-EMR on both cultured male germ cell lines and spermatozoa isolated from the mouse

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Summary

Introduction

Mobile phone usage is becoming increasingly popular worldwide and our exposure to the radiofrequencyelectromagnetic radiation (RF-EMR) emitted by these devices is unprecedented [1,2,3]. In work conducted by our group [13], it was established that RF-EMR is capable of inducing oxidative stress in purified human spermatozoa Hallmarks of this process included elevated generation of mitochondrial ROS that, in turn, resulted in impaired sperm motility and vitality, culminating in DNA fragmentation and oxidative DNA base adduct formation. Such results from cell culture studies may be viewed as highlighting the clinical importance of this area, given that the RF-EMR intensity eliciting these responses (1– 2.8 W/kg) falls comfortably within the non-damaging exposure levels currently prescribed for this form of radiation (4 W/kg). Notwithstanding these variations, a consistent theme may be emerging from studies reporting biological effects

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