There are substantial concerns that extended exposures to weak radiofrequency (RF) fields can lead to adverse health effects. In this study, HT-1080 fibrosarcoma cells were simultaneously exposed to a static magnetic flux density between 10 $$\mathrm{\mu T}$$μ T and 300 $$\mathrm{\mu T}$$μ T and RF magnetic fields with amplitudes ranging from 1 nT to 1.5 μT in the frequency range from 1.8 to 7.2 MHz for four days. Cell growth rates, intracellular pH, hydrogen peroxide, peroxynitrite, membrane potential and mitochondrial calcium were measured. Results were dependent on carrier frequency and the magnitude of the RF magnetic field, modulation frequencies and the background static magnetic field (SMF). Iron sulphur (Fe-S) clusters are essential for the generation of reactive oxygen species and reactive nitrogen species (ROS and RNS). We believe the observed changes are associated with hyperfine couplings between the chemically active electrons and nuclear spins. Controlling external magnetic fields may have important clinical implications on aging, cancer, arthritis, and Alzheimer’s.

In the last few decades, evidence has surfaced that weak radiofrequency (RF) fields can influence biological systems. This work aims to improve our understanding of how externally applied weak RF fields alter concentrations of chemical parameters that characterize oxidative stress. We conducted a series of experiments to investigate the effects of applying weak RF magnetic fields within the 3–5 MHz region on mitochondrial respiration in both human fibrosarcoma and fibroblast cells over a period of four days. Our experimental data show that RF fields between 3 and 5 MHz were able to change the modulation of mitochondrial signaling by changing the cell growth, mitochondrial mass, and oxidative stress. Exposure to RF fields at 4.2 MHz significantly increased the mitochondrial mass and oxidative stress in fibrosarcoma cells. There are substantial concerns that extended exposure to weak RF fields can lead to health effects. The ability to control these parameters by external magnetic fields may have important clinical implications.

This study explores the complex relationship between radio frequency (RF) exposure and cancer cells, focusing on the HT-1080 human fibrosarcoma cell line. We investigated the modulation of reactive oxygen species (ROS) and key antioxidant enzymes, including superoxide dismutase (SOD), peroxidase, and glutathione (GSH), as well as mitochondrial superoxide levels and cell viability. Exposure to RF fields in the 2–5 MHz range at very weak intensities (20 nT) over 4 days resulted in distinct, frequency-specific cellular effects. Significant increases in SOD and GSH levels were observed at 4 and 4.5 MHz, accompanied by reduced mitochondrial superoxide levels and enhanced cell viability, suggesting improved mitochondrial function. In contrast, lower frequencies like 2.5 MHz induced oxidative stress, evidenced by GSH depletion and increased mitochondrial superoxide levels. The findings demonstrate that cancer cells exhibit frequency-specific sensitivity to RF fields even at intensities significantly below current safety standards, highlighting the need to reassess exposure limits. Additionally, our analysis of the radical pair mechanism (RPM) offers deeper insight into RF-induced cellular responses. The modulation of ROS and antioxidant enzyme activities is significant for cancer treatment and has broader implications for age-related diseases, where oxidative stress is a central factor in cellular degeneration. The findings propose that RF fields may serve as a therapeutic tool to selectively modulate oxidative stress and mitochondrial function in cancer cells, with antioxidants playing a key role in mitigating potential adverse effects.