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Cellular Mechanisms: Oxidation

Update 6/4/23

Scientific Literature

Cellular and Biologic Mechanisms of Wireless Radiofrequency Radiation: Oxidation, Inflammation & Biomarkers

Wireless radiation has been shown in hundreds of studies to cause oxidative stress with the creation of free radicals (reactive oxygen species) in cells.  These reactive oxygen species (ROS) disrupt cell functions and damage molecules such as DNA, lipids and proteins, thus oxidative stress is a known mechanism of cell injury from EMF/EMR (see below). Antioxidants such as melatonin, zinc, vitamin C and vitamin E protect cells from injury when exposed to wireless electromagnetic frequencies (EMF). Some studies have also shown a decrease in our own internal antioxidant melatonin from EMF, thus causing increased imbalance in oxidation vs antioxidation in cellular processes, resulting in inflammation and disease.

Oxidation is process of loss of electrons from a compound or atom. When this happens, free radicals (reactive oxygen species) with an unpaired electron are created. Free radicals are highly reactive and unstable molecules.  These free radicals are desperately searching for electrons to pair up with and if none are readily available they steal them from another molecule. This creates cellular oxidative stress and if that molecule cannot neutralize the oxidation then it can be damaged.

Oxidation: The classic example of non biologic oxidation we all know is rust, whereby after adding water to iron, oxygen in the air steals electrons from iron to form iron oxide, which is identified as corrosion. Reactive oxygen species (ROS) are biologic free radical signaling molecules which are created as a normal part of cellular aerobic metabolism, a response to infection or from exposure to natural or synthetic toxicants. Overproduction of reactive oxygen species overwhelms our own antioxidant defense systems, creating oxidative stress with damage to a variety of biological macromolecules such as DNA, membrane lipids, carbohydrates and proteins.  Oxidative stress triggers inflammation. This causes a general cellular stress response with disruption of biological processes. Research indicates that this damage can be cumulative.  A metabolic signature remains and is measurable.  Physicists are now finding that spin biochemistry explains this mechanism on oxidative metabolism, ROS signaling and cellular growth. Belpomme et al has studied individuals who are electrosensitive and chemically sensitive and found similarities in biochemical analysis and inflammatory markers.

Cellular Oxidative Stress

Scientists have found that oxidative stress plays a major part in the development of chronic, degenerative and inflammatory illnesses such as cancer, autoimmune disorders, aging, cataracts, rheumatoid arthritis, cardiovascular and neurodegenerative diseases, as well as some acute pathologies (trauma, stroke).

Human Internal Antioxidants

The human body has several mechanisms to counteract oxidative stress by producing our own internal antioxidants with enzymatic (superoxide dismutase) but also non-enzymatic molecules such as alpha lipoic acid, Coenzyme Q, glutathione and. Plants also contain endogenous antioxidant defenses, such as antioxidant enzymes superoxide dismutase, catalase, and ascorbate peroxidase as well as non-enzymatic defenses including ascorbic acid, glutathione, flavonoids, carotenoids, and tocopherols, all of which scavenge and neutralize ROS. These plant antioxidants protect mammals who consume them. In humans evidence shows that vitamin E,  vitamin C, b-Carotene and melatonin may reduce the risk of inflammatory diseases such as atherosclerosis, Alzheimer’s Disease  and cancer. The delicate balance of this complex oxidant and antioxidant system is critical in the normal functioning and homeostasis of an organism.

Pollution Causes Cellular Oxidative Stress

External environmental factors found to stimulate cellular production of these unstable reactive molecules (both reactive oxygen species as well as reactive nitrogen species) include pollution, pesticides, cigarette smoke, heavy or transition metals (Cd, Hg, Pb, Fe, As), ionizing radiation and some pharmaceutical medications. Research shows that microwave radio frequencies from wireless devices also cause reactive oxygen species and reactive nitrogen species to be overproduced in cells both in animals and plants.

Mechanism of Harm from Wireless Non-ionizing Radiation is Oxidative Stress-BioInitiative Report

Yakymenko in 2016 looked at 100 currently available peer-reviewed studies on oxidative effects of low-intensity microwave radio frequencies. He found that  93 of the 100 studies confirmed that these wireless radio frequencies induced oxidative effects in biological systems. The BioInitiative Report has a full list of references accumulated by Dr. Henry Lai on RFR effects which is up to date as of March 2022.  Of 288 studies 263 showed free radical oxidative damage with exposure to RFR(91%).

Antioxidants Protect from ROS damage. Studies have also highlighted the protective effects of vitamin C, E and other antioxidants with exposure to radio frequencies. This is a complex system but the ultimate biologic result which can occur with acute exposure to higher levels or chronic exposure to lower levels of non-ionizing radiofrequencies is cumulative tissue damage. Genetic, age and health vulnerabilities influence the repair abilities of cells and thus enhance biologic harm.

Dr. Pangopolous explains in his 2021 paper the cellular basis for harm and how exposure to human‑made EMF exposure, with its modulation, pulsing and random variability, may lead to DNA damage and related pathologies, including cancer, reproductive failure and neurologic harm. He notes that human‑made electromagnetic fields (EMFs), especially in the extremely low frequency (ELF) band, and the microwave/radio frequency (RF) band which is always combined with ELF, may have synergistic effects to enhance cellular injury.

Human‐made electromagnetic fields: Ion forced‐oscillation and voltage‐gated ion channel dysfunction, oxidative stress and DNA damage (Review).  Pangopolous DJ, et al.  International Journal of Oncology. August 23, 2021.    https://pubmed.ncbi.nlm.nih.gov/34617575/

Synergistic Toxic Exposures Increase Oxidative Stress

The concern for exposure to radio frequency radiation is magnified by the fact that we are exposed to numerous pollutants in our environment on a regular basis and these toxicants can act synergistically via reactive oxygen species and other mechanisms to promote a variety of diseases.

Frequency Dependence and Toxicity 

Sharma et al (2021) Looked at the oxidative toxicity of different frequencies of RFR vs control. “Animals were exposed to 900, 1800, and 2100 MHz with the specific absorption rate (SAR) 0.434 (W/Kg), 0.433 (W/Kg), and 0.453 (W/Kg) respectively. Animal exposure was limited to 1 hour/day, 5 days/week for 1 month with a restricted power density (900 MHz- 11.638µW/m2, 1800- 11.438 µW/m2 and 2100 MHz frequency- 8.237 µW/m2).”  They concluded, ” RF-EMR exposure showed oxidative damage to the liver, increasing the incidence of brain damage in a frequency-dependent manner.Highlights EMR exposure showed frequency-dependent toxicity. Alterations in blood profile and modifications in the serological markers.Increasing lipid peroxidation indicating membrane damage.Inhibition of acetylcholinesterase activity affecting cholinergic neurotransmission.EMR exposure resulted in the loss of cellular energy and production of excess amounts of ROS thereby altering several antioxidant enzymes.Histopathological evidence of severe degenerative changes in the liver and brain.”

Sharma (2022) then looked at neurodegeneration and RFR showing a variety of effects. They took Wistar rats and  exposed them to 2100 MHz frequency for 4 h/day, 5 days/week/3 months with an estimated specific absorption rate (0.453 W/kg) and power density (8.237 µW/m2). They found,  “microwave exposure significantly increased the levels of serological triglycerides and cholesterol. Oxidative stress is observed through alteration of glutathione homeostasis followed by activated inflammatory response further confirmed by pro and anti-inflammatory cytokines in the exposed group.”  Overall conclusions were that RFR exposure caused

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