Protective Effects of Zinc on 2.45 GHz Electromagnetic Radiation-Induced Oxidative Stress and Apoptosis in HEK293 Cells

2019 · Harm · Low evidence

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HarmLow evidencePaper 1750

Compared with control, 2.45 GHz EMR exposure increased MDA and decreased SOD activity, and increased apoptotic cells and caspase-3 immunopositive cells while decreasing bcl-2. Zinc pre-treatment (50 μM or 100 μM) reduced MDA and apoptotic/caspase-3 measures a…

Study snapshot

Publicationmanual · 2019
Study typein_vitro
Reported directionHarm
Evidence ratingLow

Abstract

Protective Effects of Zinc on 2.45 GHz Electromagnetic Radiation-Induced Oxidative Stress and Apoptosis in HEK293 Cells Özsobacı NP, Ergün DD, Tunçdemir M, Özçelik D. Protective Effects of Zinc on 2.45 GHz Electromagnetic Radiation-Induced Oxidative Stress and Apoptosis in HEK293 Cells. Biol Trace Elem Res. 2019 Jul 17. doi: 10.1007/s12011-019-01811-6. Abstract Several epidemiological studies have shown that exposure to electromagnetic radiation (EMR) can be harmful to human health. The purpose of this study was to examine oxidative parameters and apoptosis induced by EMR in human kidney embryonic cells (HEK293) and to investigate whether zinc (Zn) has protective effect on EMR- induced apoptosis in HEK293 cells. For our experiment, HEK293 cells were divided into four main groups, control, EMR, 50 μM Zn + EMR, and 100 μM Zn + EMR. HEK293 cells of EMR groups were exposed to 2.45 GHz EMR for 1 h. In Zn groups, HEK293 cells were incubated with different concentrations of Zn for 48 h before EMR exposure. Oxidative stress parameters were determined by spectrophotometric method; bcl-2 and caspase-3 were assessed immunohistochemically and TUNEL method was performed for apoptotic activity. EMR group had higher malondialdehyde (MDA) level and lower superoxide dismutase (SOD) activity compared with control group. In Zn-applied groups, MDA was decreased and SOD activity was increased compared with EMR group. The number of the apoptotic cells and caspase-3 immunopositive cells at EMR group was increased significantly compared with the control group, whereas bcl-2 was decreased. Besides, Zn-treated groups showed a significant reduction in the number of apoptotic cells and caspase-3 from that of EMR group, whereas there was an increase in bcl-2 immunopositivity. Our findings show that EMR caused oxidative stress and apoptotic activation in HEK293 cells. Zn seems to have protective effects on the EMR by increasing SOD activity and bcl-2 immunopositivity, decreasing lipid peroxidation and caspas-3 immunopositivity. ncbi.nlm.nih.gov

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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.

Study typein_vitro
Effect directionharm
PopulationHEK293 (human kidney embryonic) cells
Sample sizeNot supplied
ExposureRF · 2450 MHz · 1 h (EMR exposure); Zn pre-incubation 48 h
Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Compared with control, 2.45 GHz EMR exposure increased MDA and decreased SOD activity, and increased apoptotic cells and caspase-3 immunopositive cells while decreasing bcl-2. Zinc pre-treatment (50 μM or 100 μM) reduced MDA and apoptotic/caspase-3 measures and increased SOD activity and bcl-2 relative to the EMR-only group.

Outcomes measured

  • Oxidative stress markers (malondialdehyde, superoxide dismutase activity)
  • Apoptosis (TUNEL)
  • Caspase-3 immunopositivity
  • bcl-2 immunopositivity

Limitations

  • In vitro cell model (HEK293); generalizability to humans not addressed in abstract
  • No SAR or dosimetry details reported in abstract
  • Sample size and replication details not reported in abstract
View raw extracted JSON
{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": 2450,
    "sar_wkg": null,
    "duration": "1 h (EMR exposure); Zn pre-incubation 48 h"
  },
  "population": "HEK293 (human kidney embryonic) cells",
  "sample_size": null,
  "outcomes": [
    "Oxidative stress markers (malondialdehyde, superoxide dismutase activity)",
    "Apoptosis (TUNEL)",
    "Caspase-3 immunopositivity",
    "bcl-2 immunopositivity"
  ],
  "main_findings": "Compared with control, 2.45 GHz EMR exposure increased MDA and decreased SOD activity, and increased apoptotic cells and caspase-3 immunopositive cells while decreasing bcl-2. Zinc pre-treatment (50 μM or 100 μM) reduced MDA and apoptotic/caspase-3 measures and increased SOD activity and bcl-2 relative to the EMR-only group.",
  "effect_direction": "harm",
  "limitations": [
    "In vitro cell model (HEK293); generalizability to humans not addressed in abstract",
    "No SAR or dosimetry details reported in abstract",
    "Sample size and replication details not reported in abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "2.45 GHz",
    "electromagnetic radiation",
    "RF",
    "HEK293",
    "oxidative stress",
    "apoptosis",
    "zinc",
    "MDA",
    "SOD",
    "caspase-3",
    "bcl-2",
    "TUNEL"
  ],
  "suggested_hubs": []
}
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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: 10.1007/s12011-019-01811-6
PubMed: Not supplied

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