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It remains controversial whether exposure to environmental radiofrequency signals (RF) impacts cell status or response to cellular stress such as apoptosis or autophagy. We used two label-free techniques, cellular impedancemetry and Digital Holographic Microscopy (DHM), to assess the overall cellular response during RF exposure alone, or during co-exposure to RF and chemical treatments known to induce either apoptosis or autophagy. Two human cell lines (SH-SY5Y and HCT116) and two cultures of primary rat cortex cells (astrocytes and co-culture of neurons and glial cells) were exposed to RF using an 1800 MHz carrier wave modulated with various environmental signals (GSM: Global System for Mobile Communications, 2G signal), UMTS (Universal Mobile Telecommunications System, 3G signal), LTE (Long-Term Evolution, 4G signal, and Wi-Fi) or unmodulated RF (continuous wave, CW). The specific absorption rates (S.A.R.) used were 1.5 and 6 W/kg during DHM experiments and ranged from 5 to 24 W/kg during the recording of cellular impedance. Cells were continuously exposed for three to five consecutive days while the temporal phenotypic signature of cells behavior was recorded at constant temperature. Statistical analysis of the results does not indicate that RF-EMF exposure impacted the global behavior of healthy, apoptotic, or autophagic cells, even at S.A.R. levels higher than the guidelines, provided that the temperature was kept constant.

Purpose: The present study was conducted to re-evaluate the effect of low-level 1800 MHz RF signals on RAS/MAPK activation in live cells. Material and methods: Using Bioluminescence Resonance Energy Transfer technique (BRET), we assessed the effect of Continuous wave (CW) and Global System for Mobile (GSM)-modulated 1800 MHz signals (up to 2 W/kg) on ERK and RAS kinases' activity in live HuH7 cells. Results: We found that radiofrequency field (RF) exposure for 24 h altered neither basal level of RAS and ERK activation nor the potency of phorbol-12-myristate-13-acetate (PMA) to activate RAS and ERK kinases. However, we found that exposure to GSM-modulated 1800 MHz signals at 2 W/kg decreased the PMA maximal efficacy to activate both RAS and ERK kinases' activity. Exposure with CW 1800 MHz signal at 2 W/kg only decreased maximal efficacy of PMA to activate ERK but not RAS. No effects of RF exposure at 0.5 W/kg was observed on maximal efficacy of PMA to activate either RAS or ERK whatever the signal used. Conclusions: Our results indicate that RF exposure decreases the efficiency of the cascade of events, which, from the binding of PMA to its receptor(s), leads to the activation of RAS and ERK kinases.

The rapid development of wireless communications has raised questions about their potential health risks. So far, the only identified biological effects of radiofrequency fields (RF) are known to be caused by heating, but the issue of potential nonthermal biological effects, especially on the central nervous system (CNS), remains open. We previously reported a decrease in the firing and bursting rates of neuronal cultures exposed to a Global System for Mobile (GSM) RF field at 1,800 MHz for 3 min (Moretti D, Garenne A, Haro E, Poulleier de Gannes F, Lagroye I, Lévêque P, Veyret B, Lewis N. Bioelectromagnetics 34: 571-578, 2013). The aim of the present work was to assess the dose-response relationship for this effect and also to identify a potential differential response elicited by pulse-modulated GSM and continuous-wave (CW) RF fields. Spontaneous bursting activity of neuronal cultures from rat embryonic cortices was recorded using 60-electrode multielectrode arrays (MEAs). At 17-28 days in vitro, the neuronal cultures were subjected to 15-min RF exposures, at specific absorption rates (SAR) ranging from 0.01 to 9.2 W/kg. Both GSM and CW signals elicited a clear decrease in bursting rate during the RF exposure phase. This effect became more marked with increasing SAR and lasted even beyond the end of exposure for the highest SAR levels. Moreover, the amplitude of the effect was greater with the GSM signal. Altogether, our experimental findings provide evidence for dose-dependent effects of RF signals on the bursting rate of neuronal cultures and suggest that part of the mechanism is nonthermal. NEW & NOTEWORTHY In this study, we investigated the effects of some radiofrequency (RF) exposure parameters on the electrical activity of neuronal cultures. We detected a clear decrease in bursting activity, dependent on exposure duration. The amplitude of this effect increased with the specific absorption rate (SAR) level and was greater with Global System for Mobile signal than with continuous-wave signal, at the same average SAR. Our experiment provides unique evidence of a decrease in electrical activity of cortical neuronal cultures during RF exposure.