Abstract

It has been shown that magnetic fields in the extremely low frequency range (ELF-MF) can act as a stressor in various in vivo or in vitro systems, at flux density levels below those inducing excitation of nerve and muscle cells, which are setting the limits used by most generally accepted exposure guidelines, such as the ones published by the International Commission on Non-Ionizing Radiation Protection. In response to a variety of physiological and environmental factors, including heat, cells activate an ancient signaling pathway leading to the transient expression of heat shock proteins (HSPs), which exhibit sophisticated protection mechanisms. A number of studies suggest that also ELF-MF exposure can activate the cellular stress response and cause increased HSPs expression, both on the mRNA and the protein levels. In this review, we provide some of the presently available data on cellular responses, especially regarding HSP expression, due to single and combined exposure to ELF-MF and heat, with the aim to compare the induced effects and to detect possible common modes of action. Some evidence suggest that MF and heat can act as costressors inducing a kind of thermotolerance in cell cultures and in organisms. The MF exposure might produce a potentiated or synergistic biological response such as an increase in HSPs expression, in combination with a well-defined stress, and in turn exert beneficial effects during certain circumstances.

Highlights

  • Cellular stress can be caused by a number of physical and/or chemical factors

  • OZ, MRS, MM, and MS: design the work; acquisition, analysis, or interpretation of data; drafting or revision of the work; final approval of the version to be published; agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved

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Summary

INTRODUCTION

Cellular stress can be caused by a number of physical and/or chemical factors. These include nonphysiological temperatures (heat, cold), oxygen deficits, acid–base imbalances, toxic compounds, ionizing radiation, etc. [1,2,3]. The MF exposures alone showed increased HSP70 expression levels [47, 54] When both normal (breast epithelium HBL-100 and endothelial cells from pig pulmonary arteries SPAE) and cancer cells (MCF-7 breast cancer and HeLa cervix carcinoma cells) were subjected to higher flux densities (680 μT and 34 mT) for longer exposure times (0–24 h), and were heat stressed in the range 40–44°C both concurrently and post MF exposure, again increased HSP70 mRNA levels/synthesis was seen in the coexposed samples, compared to thermally stressed samples. Under such conditions MF exposure alone did not exert any effect. Rats were stressed at 43°C for 12 min before 60 Hz MF exposure for 15, 30, and 60 days at 1 mT magnetic flux density [58], whereas in the Drosophila study, samples were concurrently heat stressed (34–37°C) and exposed to 50 Hz, 100 μT for 30 min [59]

60 Hz adenocarcinoma
50 Hz train
50 Hz 100 μT 30 min
SUMMARY AND CONCLUDING REMARKS
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