Disordered Redox Metabolism of Brain Cells in Rats Exposed to Low Doses of Ionizing Radiation or Uhf Electromagnetic Radiation

Abstract

Aim: To investigate the changes of redox-state of mammalian brain cells as the critical factor of initiation and formation of radiation damage of biological structures in setting of continuous exposure to low doses of ionizing radiation or fractionated ultra high frequency electromagnetic radiation (UHF EMR) at non-thermal levels. Materials and Methods: The influence of low-intensity ionizing radiation was studied on outbred female rats kept for 1.5 years in the Chernobyl accident zone. The effects of total EMR in the UHF band of non-thermal spectrum were investigated on Wistar rats. The rate of formation of superoxide radicals and the rate of NO synthesis in mitochondria were determined by the EPR. Results: After exposure to ionizing or UHF radiation, the levels of ubisemiquinone in brain tissue of rats decreased by 3 and 1.8 times, respectively. The content of NO-FeS-protein complexes in both groups increased significantly (р < 0.05). In the conditions of ionizing or EMR the rates of superoxide radical generation in electron-transport chain of brain cell mitochondria increased by 1.5- and 2-fold, respectively (р < 0.05). In brain tissue of rats kept in the Chernobyl zone, significant increase of NO content was registered; similar effect was observed in rats treated with UHFR (р < 0.05). Conclusions: The detected changes in the electron transport chain of mitochondria of brain cells upon low-intensity irradiation or UHF EMR cause the metabolic reprogramming of cell mitochondria that increases the rate of superoxide radical generation and nitric oxide, which may initiate the development of neurodegenerative diseases and cancer. This article is part of a Special Issue entitled “The Chornobyl Nuclear Accident: Thirty Years After”.

Adverse effect propensity: A new feature of Gulf War illness predicted by environmental exposures

“… 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 MCS, nonionizing radiation sensitivity, and ionizing radiation sensitivity involve oxidative and mitochondrial mechanisms. 44 , 45 , 46 , 47 , 48 , 49 Thus, a relationship between propensity to experience AEs to environmental factors, including radiation, and self-reported chemical sensitivity is plausible. Since mitochondrial injury may lead to ongoing oxidative stress/free radical production, 50 , 51 , 52 leading to increased competition for antioxidant defenses—and positioning mitochondrial injury further along the path toward clinical mitochondrial “threshold effects” 53 , 54 that may be triggered by a new exposure, it is plausible that specific past exposures may have contributed to enhanced risk of AE vulnerability in VGWI.…”

Identification of Plasma Lipidome Changes Associated with Low Dose Space-Type Radiation Exposure in a Murine Model

“…Several studies have contributed to the understanding of radiation induced molecular damage and tissue injury [10,11], however, there is no consensus about the health risks of low dose high-linear energy transfer (LET) radiation. Prior studies have reported oxidative stress in the central nervous system of mice due to exposure to low-LET radiation at doses <1 Gy in chronic low dose rates [12]. Other laboratories have shown behavioral deficiencies and increased cardiovascular risk associated with low dose 1 H and HZE radiation [13,14].…”

Effects of Radiofrequency Electromagnetic Radiation on Neurotransmitters in the Brain

“…The energy flux density in the exposure area was 1.0-6.0 mW/cm 2 . Ultrahigh frequency EMR resulted in a significant increase in the level of NO synthesis in the mitochondria of neural cells in animal brain tissue and a significant increase in the activity of mitochondrial NO synthase (32). Considering the toxic effect of high NO concentrations on cells, the increase in NO may cause neuronal damage, which in turn leads to a decrease in learning and memory ability in mice.…”