We have heard many times that our cell phones, wifi transmitters, satellites are safe because they transmit only non-ionizing radiation, and we have heard that only ionizing radiation causes significant chemical changes. This is not true, at least in one clear case: If non-ionizing radiation, which includes visible light, could not cause significant chemical changes in biomolecules, to put it bluntly, we’d all be blind. No animals could see visible light without the significant chemical changes caused by light hitting certain molecules in the eye and changing them. No electrons are knocked off of any molecules directly by light, no molecules may be directly ionized, but still, isometric (molecular arrangement) changes are triggered.
Non-ionizing radiation, such as ultraviolet (UV) light (and visible light!) can cause significant chemical changes in biomolecules. UV radiation is known to induce structural changes and peptide bond cleavages in proteins, leading to photoaging and photocarcinogenesis[2]. Additionally, exposure to non-ionizing electromagnetic fields has been shown to lead to the suppression of mitotic activity and a higher incidence of chromosomal aberrations in lymphocytes, indicating significant biological effects at the cellular level[3]. Unlike ionizing radiation, which can directly ionize atoms and cause severe damage to biological molecules, non-ionizing radiation primarily exerts its effects through indirect mechanisms, such as the generation of reactive oxygen species and the disruption of molecular structures[1][5]. Therefore, non-ionizing radiation can indeed cause significant chemical changes in biomolecules, albeit through different mechanisms than ionizing radiation.
Suppression of Mitotic Activity
Suppression of mitotic activity is inhibition or delay of cell division.
The suppression of mitotic activity in neural progenitors and neurons can have various consequences, including alterations in cell fate and increased neuronal apoptosis. Prolonged mitosis of neural progenitors has been shown to alter cell fate in the developing brain, and it can lead to increased neuronal apoptosis[6][8]. Additionally, recent evidence indicates that post-mitotic neurons can re-enter the cell cycle, leading to abnormal cell division and potential neuronal death[7][9][10]. These findings suggest that the suppression of mitotic activity can impact both neural progenitors and post-mitotic neurons, potentially influencing neurogenesis and neuronal survival.
Chronic Pain
Chronic pain is a complex condition that involves neuroplasticity in the somatosensory circuits of the spinal cord, thalamus, and cortex. The development and maintenance of chronic pain are associated with alterations in synaptic modifications and transmission, which contribute to the pathophysiology of pain. Microglia and astrocytes play a crucial role in modulating neuropathic pain by inducing and modulating cellular responses and signaling pathways.
The suppression of mitotic activity can lead to alterations in synaptic modifications and transmission. Research suggests that mitotic kinesins, which are involved in cell division, also play a vital role in synaptic transmission[11]. Synaptic transmission is a complex process that relies on spatially and temporally coordinated multistep processes, allowing for neuronal communication and activity-dependent changes in synaptic strength[12]. Studies have shown that electrophysiological analysis of synaptic transmission in model systems like Drosophila can provide insights into the dynamic and plastic nature of synaptic transmission, which is highly regulated at the presynaptic and postsynaptic levels[13]. Additionally, research has demonstrated that certain kinesins, such as Kif11 and Kif21B, act as inhibitory constraints on excitatory synaptic transmission in post-mitotic neurons[14]. Furthermore, the combination of NGN2 programming with developmental patterning has been shown to generate human excitatory neurons with NMDAR-mediated synaptic transmission, highlighting the intricate relationship between mitotic activity and synaptic function[15].
Summary
Non-ionizing radiation is a type of electromagnetic radiation that does not have enough energy to remove tightly bound electrons from atoms or molecules, causing ionization. However, it can still cause significant chemical changes in biomolecules.
One example of non-ionizing radiation that can cause chemical changes in biomolecules is ultraviolet (UV) radiation. UV radiation has enough energy to excite electrons in biomolecules, leading to the formation of reactive oxygen species (ROS) such as singlet oxygen and free radicals. These ROS can then react with biomolecules, such as DNA, proteins, and lipids, causing chemical modifications.
UV radiation-induced DNA damage is of particular concern, as it can lead to mutations in the genetic material. These mutations can disrupt normal cellular processes, potentially leading to the development of cancer. UV radiation can also modify proteins and lipids, altering their structure and function.
Another type of non-ionizing radiation that can cause chemical changes in biomolecules is visible light. Visible light can induce photochemical reactions in certain molecules, such as retinal in the eye’s photoreceptor cells. This allows us to see, but it can also lead to the formation of toxic byproducts that can damage biomolecules.
In addition to UV radiation and visible light, other forms of non-ionizing radiation, such as infrared radiation and radiofrequency radiation, can also cause chemical changes in biomolecules. These changes may result from the absorption of energy by biomolecules, leading to structural modifications or altered biochemical reactions.
While non-ionizing radiation does not directly cause ionization, it can still have significant effects on biomolecules through chemical modifications. These changes can disrupt normal cellular processes, potentially leading to various health effects, including DNA damage, protein dysfunction, and lipid alterations. Understanding the effects of non-ionizing radiation on biomolecules is essential for assessing the potential risks associated with exposure to these types of radiation.
Citations:
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4060780/
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8616186/
[3] https://www.sciencedirect.com/science/article/pii/S0079610718301007
[4] https://www.nrc.gov/reading-rm/basic-ref/students/for-educators/09.pdf
[5] https://courses.lumenlearning.com/chemistryformajors/chapter/biological-effects-of-radiation-2/
[6] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4706996/
[7] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4418291/
[8] https://www.sciencedirect.com/science/article/pii/S089662731501079X
[9] https://www.nature.com/articles/s41598-019-40462-4
[10] https://journals.plos.org/plosgenetics/article?id=10.1371%2Fjournal.pgen.1003049
[11] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7827351/
[12] https://www.sciencedirect.com/topics/immunology-and-microbiology/synaptic-transmission
[13] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5980642/
[14] https://www.nature.com/articles/s41598-018-35634-7
[15] https://www.sciencedirect.com/science/article/pii/S2211124718306259
