Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the HEK293 cells.
← Research streamCompared with control, 2.4 GHz EMF exposure increased MDA and apoptosis/caspase-3 and decreased SOD and GSH-Px activities and bcl-2. Selenium pre-incubation (100 or 200 nM for 48 h) before EMF exposure reduced MDA and apoptosis/caspase-3 and increased SOD, GS…
Study snapshot
Abstract
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 peroxidation, 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.
AI evidence extraction
Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.
Main findings
Compared with control, 2.4 GHz EMF exposure increased MDA and apoptosis/caspase-3 and decreased SOD and GSH-Px activities and bcl-2. Selenium pre-incubation (100 or 200 nM for 48 h) before EMF exposure reduced MDA and apoptosis/caspase-3 and increased SOD, GSH-Px, and bcl-2 relative to EMF alone.
Outcomes measured
- Oxidative stress markers (MDA, SOD activity, GSH-Px activity)
- Apoptosis
- Caspase-3
- Bcl-2
Limitations
- No sample size reported in abstract
- SAR/dosimetry details not reported in abstract
- Only an in vitro cell model (HEK293)
- Exposure duration limited to 1 h
View raw extracted JSON
{
"study_type": "in_vitro",
"exposure": {
"band": "RF",
"source": null,
"frequency_mhz": 2400,
"sar_wkg": null,
"duration": "1 h"
},
"population": "HEK293 (human embryonic kidney) cells",
"sample_size": null,
"outcomes": [
"Oxidative stress markers (MDA, SOD activity, GSH-Px activity)",
"Apoptosis",
"Caspase-3",
"Bcl-2"
],
"main_findings": "Compared with control, 2.4 GHz EMF exposure increased MDA and apoptosis/caspase-3 and decreased SOD and GSH-Px activities and bcl-2. Selenium pre-incubation (100 or 200 nM for 48 h) before EMF exposure reduced MDA and apoptosis/caspase-3 and increased SOD, GSH-Px, and bcl-2 relative to EMF alone.",
"effect_direction": "mixed",
"limitations": [
"No sample size reported in abstract",
"SAR/dosimetry details not reported in abstract",
"Only an in vitro cell model (HEK293)",
"Exposure duration limited to 1 h"
],
"evidence_strength": "low",
"confidence": 0.78,
"peer_reviewed_likely": "yes",
"keywords": [
"2.4 GHz",
"RF-EMF",
"HEK293",
"selenium",
"oxidative stress",
"MDA",
"SOD",
"GSH-Px",
"apoptosis",
"caspase-3",
"bcl-2"
],
"suggested_hubs": []
}AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.
Identifiers and source
DOI: 10.1016/j.jtemb.2018.04.008
PubMed: 29685784
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