Effects of Single and Repeated Exposure to a 50-Hz 2-mT Electromagnetic Field on Primary Cultured Hippocampal Neurons

Abstract

The prevalence of domestic and industrial electrical appliances has raised concerns about the health risk of extremely low-frequency magnetic fields (ELF-MFs). At present, the effects of ELF-MFs on the central nervous system are still highly controversial, and few studies have investigated its effects on cultured neurons. Here, we evaluated the biological effects of different patterns of ELF-MF exposure on primary cultured hippocampal neurons in terms of viability, apoptosis, genomic instability, and oxidative stress. The results showed that repeated exposure to 50-Hz 2-mT ELF-MF for 8 h per day after different times in culture decreased the viability and increased the production of intracellular reactive oxidative species in hippocampal neurons. The mechanism was potentially related to the up-regulation of Nox2 expression. Moreover, none of the repeated exposure patterns had significant effects on DNA damage, apoptosis, or autophagy, which suggested that ELF-MF exposure has no severe biological consequences in cultured hippocampal neurons.

Manmade Electromagnetic Fields and Oxidative Stress—Biological Effects and Consequences for Health

“…It is important to note that tumor cells often have an intrinsically disturbed oxidative balance and may, therefore, react differently to EMF or other treatments than a normal cell. However, primary neurons from the brain also reacted to repeated 50 Hz ELF-MF exposure at a flux density of 2 mT by an increased production of ROS, an upregulation of the NADPH oxidase NOX2, and faster neuronal cell death, especially pronounced in older cell cultures [ 75 ]. This indicates that the findings from the experiments with tumor cells are at least partially transferable to normal and immortalized cells.…”

“…It seems that the degree of cell differentiation or age is critical; cells that were further differentiated generally were less sensitive compared to undifferentiated cells or cells in an early stage of differentiation [ 75 , 82 , 84 , 85 ]. It is noteworthy that the induction of ROS and signs of oxidative stress appear to be more reproducible in neural cells exposed to ELF-MF than to RF-EMF [ 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 92 , 93 , 94 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 113 ]. Higher doses of RF-EMF exposure mostly resulted in more pronounced effects, although not consistently, and a temperature increase or other confounders cannot always be excluded [ 92 , 93 , 96 , 99 , 100 , 101 , 102 , 103 ].…”

“…The extent of induction, as well as the possibility of counter-regulation has to be considered, presumably requiring a threshold level or persistence to translate to health impairment. It seems that the degree of cell differentiation or age is critical; cells that were further differentiated generally were less sensitive compared to undifferentiated cells or cells in an early stage of differentiation [75,82,84,85]. It is noteworthy that the induction of ROS and signs of oxidative stress appear to be more reproducible in neural cells exposed to ELF-MF than to RF-EMF [75][76][77][78][79][80][81][82][92][93][94][96][97][98][99][100][101][102][103][104][105]113].…”

Overexpression of Purinergic P2X4 Receptors in Hippocampus Rescues Memory Impairment in Rats with Type 2 Diabetes

“…So, we determined whether DNA damage is responsible for the P2X4R downregulation. Several methods can be used to detect DNA damage, such as the cH2AX signal [37], but they are all global tests. We used LA-PCR, a newly-developed technology, to precisely detect DNA damage on one specific gene [38].…”

Diffuse Intrinsic Pontine Gliomas Exhibit Cell Biological and Molecular Signatures of Fetal Hindbrain-Derived Neural Progenitor Cells

“…Thus, PPCs are desirable normal control cells for DIPG, and have the potential to model DIPG after transformed by DIPG-specific oncogenes. With the assistance of this tool, it will be possible to dissect the different responses of tumor cells and normal cells to multimodality therapies, including not only targeted pharmacological therapies [24] but also the physical therapies [25], and kill the tumor cells specifically without damage to normal cells. Besides functioning as normal controls for DIPG research, the application of PPCs may extend to the treatment of DIPG.…”