Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats
Mobile phone providers use electromagnetic radiation (EMR) with frequencies ranging from 900 to 1800 MHz. The increasing use of mobile phones has been accompanied by several potentially pathological consequences, such as neurological diseases related to hippocampal (HIPPON) and dorsal root ganglion neuron (DRGN). The TRPV1 channel is activated different stimuli, including CapN, high temperature and oxidative stress. We investigated the contribution TRPV1 to mitochondrial oxidative stress and apoptosis in HIPPON and DRGN following long term exposure to 900 and 1800 MHz in a rat model. Twenty-four adult rats were equally divided into the following groups: (1) control, (2) 900 MHz, and (3) 1800 MHz exposure. Each experimental group was exposed to EMR for 60 min/ 5 days of the week during the one year. The 900 and 1800 MHz EMR exposure induced increases in TRPV1 currents, intracellular free calcium influx (Ca2+), reactive oxygen species (ROS) production, mitochondrial membrane depolarization (JC-1), apoptosis, and caspase 3 and 9 activities in the HIPPON and DRGN. These deleterious processes were further increased in the 1800 MHz experimental group compared to the 900 MHz exposure group. In conclusion, mitochondrial oxidative stress, programmed cell death and Ca2+ entry pathway through TRPV1 activation in the HIPPON and DRGN of rats were increased in the rat model following exposure to 900 and 1800 MHz cell frequencies. Our results suggest that exposure to 900 and 1800 MHz EMR may induce a dose-associated, TRPV1-mediated stress response.
KeywordsApoptosis Dorsal root ganglion Hippocampus Mobile phone frequency Oxidative stress TRPV1 cation channel
Intracellular free calcium ion
Dorsal root ganglion neuron
Polyunsaturated fatty acid
Reactive oxygen species
Specific absorption rate
Transient receptor potential
Transient receptor potential vanilloid 1
Voltage gated calcium channel
The abstract of the study was published in the Thermal Biology 2017 International Symposium, September 4, 2017, Kyoto, Japan. The authors wish to thank the technician Fatih Şahin (BSN Sağlık Analiz, ARGE, Danışmanlık, Sağlık ve Tarım Ltd., Isparta, Turkey) and Dr. Nady Braidy (School of Psychiatry, Faculty of Medicine, University of New South Wales, Randwick Australia) for helping with the patch-clamp analyses and polishing English, respectively.
MN formulated the present hypothesis and was responsible for writing the report. KE, FU and SA were responsible for analyses of spectrofluorometer and plate reader.
Compliance with ethical standards
None of the authors have any to disclose. All authors approved the final manuscript.
There is no financial support for the current study.
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