Excerpt:

Published October 2024-11-02

Antioxidants 2024, 13(10), 1237; https://www.mdpi.com/2076-3921/13/10/1237 

Frequency-Dependent Antioxidant Responses in HT-1080 Human Fibrosarcoma Cells Exposed to Weak Radio Frequency Fields 

Hakki Gurhan and Frank Barnes 

Department of Electrical, Computer and Energy Engineering, University of Colorado Boulder, USA 

Abstract 

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. 

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Conclusions 

Our findings reveal that RF exposure at specific frequencies distinctly modulates the activities of key antioxidant enzymes, such as SOD and peroxidase, as well as GSH levels. This modulation underscores the dual role of SODs in controlling ROS damage and regulating ROS signaling, as detailed by Wang et al. [72]. By balancing ROS production and detoxification, SODs are crucial in maintaining cellular homeostasis and influencing cancer cell behavior. At 2.5 MHz, we observed significant oxidative stress, indicated by increased SOD activity and substantial GSH depletion, suggesting that hyperfine resonance effects at this frequency may amplify superoxide radical production, requiring a heightened antioxidant response. In contrast, exposure at 4 MHz led to a robust antioxidant response, characterized by elevated SOD and GSH levels and decreased H₂O₂. This coincided with an increase in cell viability and decreased mitochondrial superoxide, indicating enhanced mitochondrial function and an optimized balance between ROS production and antioxidant defenses in cancer cells. These frequency-dependent effects imply the involvement of hyperfine resonance interactions with mitochondrial metalloproteins, significantly impacting ROS dynamics. This modulation of ROS and apoptosis mirrors findings where RF-EMF exposure altered NADPH homeostasis and reduced superoxide levels, contributing to cell survival [73]. The potential for antioxidants to mitigate RF-induced oxidative stress underscores the need for further research into antioxidant therapies. 

At an applied RF field intensity of 20 nT, our conclusions align with a broader body of evidence suggesting that low-intensity electromagnetic fields exert biological effects through non-thermal mechanisms [74]. Furthermore, concerns have been raised about the impact of RF field intensities below current safety standards, particularly for sensitive populations. While current exposure standards are primarily based on avoiding thermal effects, increasing evidence indicates that non-thermal influences of RF fields can modulate oxidative stress, ROS production, and other cellular processes [75]. Such findings call attention to the importance of re-evaluating these standards. 

Investigating the therapeutic potential of combining RF exposure with antioxidant or pro-oxidant treatments could advance our understanding of how RF fields modulate cellular redox states. These findings suggest that frequency-specific RF exposure may selectively influence cancer cell oxidative stress, potentially improving the efficacy of conventional cancer therapies. Certain RF frequencies can either increase or decrease superoxide and other oxidative stress markers, thereby altering the balance between ROS production and antioxidant defenses. By increasing the susceptibility of cancer cells to oxidative damage, RF exposure could make them more vulnerable to treatments like chemotherapy or radiation, which depend on inducing oxidative stress. These mechanisms may also be relevant to age-related diseases, as oxidative stress is a shared factor in both cancer and aging, where mitochondrial dysfunction and ROS overproduction contribute to cellular decline, as noted by Hajam et al. [76]. Furthermore, the concept of mitohormesis, as described by Ristow [77], suggests that controlled ROS levels can trigger adaptive responses that protect cells from damage, thereby supporting longevity and healthy aging. 

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