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.

An RF Safe post argues that a 2018 review on EMF-related oxidative stress supports a mechanistic chain from radiofrequency (RF-EMF) exposure to mitochondrial reactive oxygen species (ROS) increases and downstream inflammation, emphasizing non-thermal exposures. It highlights the review’s focus on mitochondrial electron transport chain complexes I and III and discusses calcium signaling disruptions, then connects these to the site’s “Ion Timing Fidelity” model involving voltage-gated channel timing (S4 segment). The post also cites in-vitro human sperm research and other reviews as consistent with mitochondrial oxidative stress effects, while noting gaps in standardized human studies.

This animal and in vitro study examined non-thermal 900 MHz RF-EMF exposure during prenatal and postnatal development at 0.08 and 0.4 W/kg SAR. The authors report changes consistent with altered neurodevelopment, including reduced BDNF, reduced in vivo cell proliferation, and disrupted synaptic balance in rat pup brain regions. In vitro, exposed neural stem cells showed increased apoptosis and DNA double-strand breaks and shifts in cell populations toward glial lineages. The authors conclude that regulatory-level 900 MHz exposure can disrupt key neurodevelopmental processes in rodents.

This rat study examined whether pulse-modulated 900 MHz and 1800 MHz RF exposure affects blood-brain barrier permeability using Evans blue dye. The abstract reports increased permeability in male rats at both frequencies (stronger at 1800 MHz) and in female rats at 900 MHz but not at 1800 MHz. The authors suggest mobile-phone-like RF exposure could increase blood-brain barrier permeability under non-thermal conditions, while noting that further mechanistic studies are needed.