Abstract

Presently, there is a rise in the use of mobile phones, laptops, and wireless internet technologies such as Wi-Fi and 5G routers/modems across the globe; these devices emit a considerable amount of electromagnetic radiation (EMR) which could interact with the male reproductive system either by thermal or nonthermal mechanisms. The aim of this review was to examine the effects of mobile phone use on male fertility. Related studies that reported on the effects of EMR from mobile phones on male fertility from 2003 to 2020 were evaluated. PubMed database was used. The Medical Subject Heading system was used to extract relevant research studies from PubMed. Based on the outcomes of both human and animal studies analyzed in this review, animal and human spermatozoa exposed to EMR emitted by mobile phones had reduced motility, structural anomalies, and increased oxidative stress due to overproduction of reactive oxygen species. Scrotal hyperthermia and increased oxidative stress might be the key mechanisms through which EMR affects male fertility. However, these negative effects appear to be associated with the duration of mobile phone use.

Excerpt

Recent findings from human experimentation

Long-term exposure to EMR emitted by mobile phones and Wi-Fi devices, might play a role in male infertility because of an increased production of ROS in exposed cells [Figures ​[Figures22–​-55].[16]

https://europepmc.org/article/MED/33311902

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Abstract

Artificially generated radiofrequency-electromagnetic energy (RF-EME) is now ubiquitous in our environment owing to the utilization of mobile phone and Wi-Fi based communication devices. While several studies have revealed that RF-EME is capable of eliciting biological stress, particularly in the context of the male reproductive system, the mechanistic basis of this biophysical interaction remains largely unresolved. To extend these studies, here we exposed unrestrained male mice to RF-EME generated via a dedicated waveguide (905 MHz, 2.2 W/kg) for 12 h per day for a period of 1, 3 or 5 weeks. The testes of exposed mice exhibited no evidence of gross histological change or elevated stress, irrespective of the RF-EME exposure regimen. By contrast, 5 weeks of RF-EME exposure adversely impacted the vitality and motility profiles of mature epididymal spermatozoa. These spermatozoa also experienced increased mitochondrial generation of reactive oxygen species after 1 week of exposure, with elevated DNA oxidation and fragmentation across all exposure periods. Notwithstanding these lesions, RF-EME exposure did not impair the fertilization competence of spermatozoa nor their ability to support early embryonic development. This study supports the utility of male germ cells as sensitive tools with which to assess the biological impacts of whole-body RF-EME exposure.

Summary

In summary, our evidence supports the hypothesis that sustained whole-body RF-EME is capable of inducing a state of oxidative stress in the male germ line, a cell vulnerable to the effects of ROS. Furthermore, our data further implicate the mitochondria as the target for RF-EME biophysical interaction, with a consequential elevation of mitochondrial ROS generation being linked to reduced motility and elevated oxidative DNA damage and DNA fragmentation in the spermatozoa of exposed males. Whilst these lesions were not sufficient to compromise fertilization competence or early embryo development, it will nonetheless be of interest to investigate the transgenerational influence of whole-body RF-EME in future studies.

https://www.nature.com/articles/s41598-019-53983-9

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Brendan J. Houston

Brett Nixon

R J. Aitken

Geoffry N. De Iuliis

• ¹School of Environmental and Life Sciences, Discipline of Biological Sciences, University of Newcastle, Australia
• ²School of Mathematical and Physical Sciences, University of Newcastle, Australia

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 W/kg 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 hours 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.

Keywords: RF-EMF, Spermatozoa, Oxidative damage, Germ Cells, Mitochondria, DNA Damage, Mobile phone radiation

Received: 19 Dec 2017; Accepted: 29 Aug 2018.

Copyright: © 2018 Houston, Nixon, King, Aitken and De Iuliis. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Geoffry N. De Iuliis, University of Newcastle, School of Environmental and Life Sciences, Discipline of Biological Sciences, Callaghan, 2308, NSW, Australia, geoffry.deiuliis@newcastle.edu.au

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