4.3 Article Proceedings Paper

Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the HEK293 cells

Journal

JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY
Volume 50, Issue -, Pages 572-579

Publisher

ELSEVIER GMBH
DOI: 10.1016/j.jtemb.2018.04.008

Keywords

Selenium; Electromagnetic field; Oxidative stress; Apoptosis; HEK 293

Funding

  1. Research Fund of Istanbul University [51182, 24522]

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There is a widespread use of 2.4 GHz electromagnetic radiation emitting devices especially in communication and education. Recent studies show the adverse effects of electromagnetic fields (EMF) such as oxidative stress, cellular damage and apoptosis on tissues. Selenium (Se) has an antioxidant properties by inhibiting oxidative damage being within the structure of antioxidant enzymes like glutathione peroxidase (GSH-Px) and it has also regulatory function for cell cycle and apoptosis. The aim of this study was to investigate the effect of Se on 2.4 GHz frequency EMF exposed human embryonic kidney cells (HEK293) by means of alterations in apoptotic and oxidative stress parameters. Our study was planned as control, EMF, 100 nM Se + EMF, 200 nM Se + EMF groups. EMF groups were exposed to 2.4 GHz EMF for 1 h, element groups were incubated with two different doses of Se added cell culture medium for 48 h before EMF exposure. MDA levels were significantly higher whereas SOD and GSH-Px activities were significantly lower in EMF compared to control. 100 and 200 nM Se + EMF application decreased MDA levels, increased SOD and GSH-Px activities than EMF. Apoptosis and caspase-3 were statistically significantly higher but bcl-2 was lower in EMF than control. Apoptosis and caspase-3 were lower in 100 and 200 nM Se + EMF, although bcl-2 were higher than EMF. In conclusion, Se has protective effects against 2.4 GHz EMF-induced oxidative stress by reducing lipid per oxidation, regulating SOD and GSH-Px activity. Also, Se has inhibitory effect on 2.4 GHz EMF induced apoptosis by increasing the expression of anti-apoptotic protein bcl-2 and suppressing apoptosis regulatory protein caspase-3.

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