This PubMed-listed in vitro study tested whether 1800 MHz RF-EMF exposure can modify chemically induced DNA damage in mouse embryonic fibroblasts under standardized, non-thermal conditions. The authors report RF-EMF alone did not produce detectable DNA damage and did not significantly increase damage from hydrogen peroxide, 4-nitroquinoline-1-oxide, or cadmium. However, co-exposure with hexavalent chromium (Cr(VI)) was reported to synergistically increase DNA damage in the comet assay, which the authors interpret as possible selective exacerbation of Cr(VI)-induced genotoxicity requiring further investigation.

This in vitro study examined strictly non-thermal, GSM-like 3.5 GHz RF-EMF exposure in cultured mouse dorsal root ganglion neurons for 1–24 hours. The authors report time-dependent reductions in cell viability alongside increased ROS and changes consistent with mitochondria-mediated apoptosis (e.g., Bax/caspase-3 up, cytochrome c release, Bcl-2 down) and increased p75NTR. They conclude these findings provide mechanistic evidence of peripheral neuronal vulnerability to mid-band RF exposure and call for further in vivo research.

This in vitro study tested whether 1800 MHz RF-EMF modifies chemically induced DNA damage in mouse embryonic fibroblasts under non-thermal exposure conditions. RF-EMF alone did not produce detectable DNA damage and did not significantly enhance damage from hydrogen peroxide, 4NQO, or cadmium. In contrast, co-exposure with hexavalent chromium (Cr(VI)) was reported to synergistically increase DNA damage, suggesting a selective co-genotoxic interaction under specific chemical conditions.

This RF Safe article argues that pulsed, low-frequency-modulated wireless radiofrequency exposures could disrupt voltage-gated ion channel timing (via the S4 voltage sensor), leading to altered immune-cell signaling, mitochondrial oxidative stress, and downstream innate immune activation and inflammation. It presents a mechanistic narrative linking small membrane-potential shifts to changes in calcium and proton channel behavior, then to mitochondrial reactive oxygen species and inflammatory pathways (e.g., cGAS–STING, TLR9, NLRP3). The post cites animal findings and a described 2025 mouse gene-expression study as supportive, but the piece itself is not a peer-reviewed study and some claims are presented as deterministic without providing full methodological details in the excerpt.

This RF Safe article argues that persistent low-intensity, pulsed RF exposure could disrupt the timing of voltage-gated ion channel activity by affecting the S4 voltage-sensing region, leading to downstream changes in calcium/proton signaling, mitochondrial stress, and immune dysregulation. It proposes a mechanistic chain from altered ion gating to increased mitochondrial ROS, mitochondrial DNA release, and activation of innate immune pathways (e.g., cGAS-STING, TLR9, NLRP3). The post cites “multiple reviews and experiments” and references animal findings and a 2025 mouse study, but the provided text does not include enough study details to independently assess the strength of the evidence.

This in vitro study used LC-MS metabolomics to assess how continuous versus intermittent RF-EMF irradiation affects mouse Leydig (TM3) and spermatogonia (GC-1) cells. The authors report stronger metabolic disturbances in TM3 cells under continuous exposure, including changes in amino acid and glutathione-related pathways, while intermittent exposure mainly affected fatty acyl and purine-related metabolism. GC-1 cells were reported to be less sensitive, and ADP changes were proposed as a potential metabolic signature. The authors interpret these metabolic disturbances as suggesting potential reproductive health risks.

This mouse study examined whether cell phone radiation affects T lymphocytes over 2–8 weeks of exposure. CD4 and CD8 subset percentages were similar across groups, but after more than six weeks, exposed groups showed increased T-cell apoptosis and reduced transformation rates compared with shams. The study also reports decreased IL-10 and increased IL-12 in exposed groups, suggesting time-dependent immunological changes under the tested conditions.

This in vitro study exposed BV2 mouse microglial cells to 3.5 GHz EMF for 2 hours and reports reduced cell growth and increased apoptosis alongside oxidative stress and signaling changes. The authors report that ROS generation and activation of JNK-1/2 and p38 MAPK were key events in the observed cytotoxicity. Polydeoxyribonucleotide (PDRN) reportedly reduced several EMF-associated cytotoxicity markers, suggesting a potential mitigating effect under the tested conditions.

This animal study reports that prolonged RF-EMR exposure (2.45 GHz for 8 weeks) increased oxidative stress and ferroptosis in mouse testicular tissue and was associated with reduced sperm quality. Melatonin administration reportedly mitigated oxidative injury and inhibited ferroptosis. The abstract attributes the protective effect to Nrf2 pathway activation via MT1/MT2 receptors.

This review summarizes reported biological effects of extremely low frequency (ELF) electric and magnetic fields, describing them as significant and often acting as stressors. Reported outcomes include metabolic, hormonal, and body weight changes in rodents, lethality at high exposure levels in mice and insects, and increased mitotic index in mouse tissues/cells under specified exposure conditions. The review suggests many effects may be mediated through neuroendocrine, nervous system, or behavioral responses to field exposure.