EMF and the brain

2021 Frontiers

Cuicui Hu, Hongyan Zuo, Yang Li

“Some studies have suggested that the calcium activation could be the initial event leading to alteration in protein configuration, followed by generation of ROS and ultimately activation of the molecular apoptosis pathways.

Lushchak et al. reported that EMR exposure may firstly produce the free radicals in the brain and later they are converted to ROS. The elevation of ROS level can attack various biomolecules in the cell. The raised ROS can also in turn trigger calcium release, and then activate the genetic factors leading to DNA damage.

Any alteration in gene and enzyme levels, may result in the activation of downstream signaling, particularly the mitochondria-dependent caspase-3 pathway can cause the apoptosis of neurons, which would lead to altered behavioral manifestations and pathophysiological changes in the brain.

In a word, EMR exposure does increases the intracellular calcium and the formation of ROS, which would alter the cellular function eventually and lead to numerous biological effects including neurotransmitter imbalance. “

• “It is known that membrane is the first and an important target of EMF in cells. Cell membrane damage might result in neurotransmitter changes in the brain.”
• “EMR can alter cell membrane permeability such as changes in calcium, ionic distribution and ion permeability”.
• “Calcium is one of the important signaling substances, and an imbalance of calcium homeostasis can alter many functions of the cell.  It was reported that the number of opened calcium channel increased with the presence of EMFs, which might resulting in the increased intracellular calcium concentration under EMR exposure. In addition, the changes of intracellular calcium levels can trigger unusual synaptic action or cause neuronal apoptosis. This in turn can exert an influence on the neurotransmission of learning and memory process”.
• It was reported that, EMR activation of voltage-gated calcium channels (VGCCs) causes a rapid increase in intracellular calcium, nitric oxide, and peroxynitrite.
• “The changes of membrane permeability may result in the damage of membrane integrity, and lead to the changes in brain neurotransmitter imbalance.”
• “It is known that neurotransmitter and its receptors are involved in various signaling related to cell proliferation, apoptosis, differentiation and inflammation. The crosstalk between neurotransmission and cell signaling may in turn affect the metabolism and transport of neurotransmitters. EMR exposures produce the main pathophysiological effects via excessive calcium signaling and the peroxynitrite pathway, and the diverse non-thermal effects of EMR are produced via VGCC activation”.
• “As the energy source of the cell, the mitochondrial calcium reaction was influenced by the alterations in calcium signaling pathways in response to the effects of EMR exposure”.
• “In addition to calcium signaling changes, EMR can cause activation of free radical processes and overproduction of reactive oxygen species (ROS) in neurons. Due to the dependent on oxidative phosphorylation for energy, neurons are vulnerable for oxidative stress compared to other cells. During EMR exposure, the occurrence of oxidant-antioxidant imbalance in the brain leads to oxidative stress”.
• ” The various oxidants act to produce greatly elevated NF-kappa B (NF-κB) activity, leading to inflammation. In addition, NF-κB signaling is reported to be involved in neural immune response, synaptic plasticity, learning and memory, neuroprotection and neurodegeneration.”
• “It has been shown that EMR exposure leads to up-regulated elements belonging to apoptotic pathways, which results in neuronal apoptosis. The probable mechanisms are mainly attributed to increased ROS generation following EMR exposure.”
• “The energy of non-ionizing radiation is not enough to directly break chemical bonds, and therefore the occurrence of DNA damage with non-ionizing EMR exposures is primarily a consequence of generation of ROS, followed by oxidative stress. Numerous animal experiments have clearly demonstrated that non-thermal EMR can cause oxidative stress, particularly in the brain”.
• “It has been documented that non-thermal EMR exposure of 900 MHz or 2.45 GHz in rats, either short-term or long-term, can trigger neuronal dysfunction and apoptosis of hippocampal pyramidal cells and cerebellum Purkinje cells through induction of oxidative stress.”
• “ROS plays a key role in the regulation of cytosolic calcium homeostasis. The protein phosphorylation and activation of the AP-1 family factors and nuclear factor kappa B (NF-κB) is regulated by the level of cytosolic calcium. Activation of the protein kinases pathways regulates the physiological response to EMR exposure including neurotransmitter imbalance, but the detailed mechanisms are still unclear.”
• “Many evidences indicate that EMR alter several aspects of calcium function in cells.”
• “Though we narrow down to biochemical imbalance to simplify explanation for changes of each neurotransmitter, the combined effects of neurotransmitters still deserves attention. It is also possible that the various neurotransmission effects following EMR exposure in animals might be due to combined effects in various brain regions, such as neurophysiological changes, increase of calcium and ROS, and thereby cell membrane damage and the downstream signaling changes. An imbalance in the excitation-inhibition imbalance of neurons resulting from neurotransmitter changes, would alter behavior”.
• “Consequently, the regulation of neural circuits may be involved in the neurotransmitter disorder of the brain induced by EMR.”

Links:

https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2021.691880/full