Abstract

The continuously increasing usage of cell phones has raised concerns about the adverse effects of microwave radiation (MWR) emitted by cell phones on health. Several in vitro and in vivo studies have claimed that MWR may cause various kinds of damage in tissues. The aim of this study is to examine the possible effects of exposure to low-intensity MWR on DNA and oxidative damage in the livers of rats. Eighteen Sprague-Dawley male rats were divided into three equal groups randomly (n = 6). Group 1 (Sham-control): rats were kept under conditions the same as those of other groups, except for MWR exposure. Group 2: rats exposed to 1800 MHz (SAR: 0.62 W/kg) at 0.127 ± 0.04 mW/cm² power density, and Group 3: rats exposed to 2,100 MHz (SAR: 0.2 W/kg) at 0.038 ± 0.03 mW/cm² power density. Microwave application groups were exposed to MWR 2 h/day for 7 months. At the end of the exposure period, the rats were sacrificed and DNA damage, malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), and total oxidant-antioxidant parameter analyses were conducted in their liver tissue samples. It was found that 1800 and 2100 MHz low-intensity MWR caused a significant increase in MDA, 8-OHdG, total oxidant status, oxidative stress index, and comet assay tail intensity (P < 0.05), while total antioxidant status levels (P < 0.05) decreased. The results of our study showed that whole-body exposure to 1800 and 2100 MHz low-intensity MWR emitted by cell phones can induce oxidative stress by altering oxidant-antioxidant parameters and lead to DNA strand breaks and oxidative DNA damage in the liver of rats. Bioelectromagnetics. © 2020 Bioelectromagnetics Society.

https://pubmed.ncbi.nlm.nih.gov/33368426/

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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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