Do 50/60 Hz magnetic fields influence oxidative or DNA damage responses in human SH-SY5Y neuroblastoma cells?

International journal of radiation biology · 2022 · Mixed · Low evidence

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MixedLow evidencePaper 881

Study snapshot

PublicationInternational journal of radiation biology · 2022

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

Do 50/60 Hz magnetic fields influence oxidative or DNA damage responses in human SH-SY5Y neuroblastoma cells? Ehab Mustafa, Leonardo Makinistian, Jukka Luukkonen, Jukka Juutilainen, Jonne Naarala. Do 50/60 Hz magnetic fields influence oxidative or DNA damage responses in human SH-SY5Y neuroblastoma cells? Int J Radiat Biol. 2022 Mar 23;1-35. doi: 10.1080/09553002.2022.2055803. Abstract Purpose: We investigated possible effects of 50 Hz and 60 Hz magnetic fields (MFs) on reactive oxygen species (ROS) production, DNA damage, DNA damage repair rate, as well as gene expression related to oxidative stress and DNA damage signaling. Materials and methods: Human SH-SY5Y neuroblastoma cells were sham-exposed or exposed to 100 µTRMS MFs for 24 h, then assayed or further treated with 100 µM menadione for 1 h before the assay. The levels of ROS and cytosolic superoxide anion (O2•-) were assayed fluorometrically. DNA damage and gene expression were assayed by comet assay and RT-qPCR, respectively. To examine whether MFs affected DNA damage repair rate, cells were allowed to repair their DNA for 1 or 2 h after menadione treatment and then assayed for DNA damage. Results: There was suggestive evidence of a general low-magnitude increase in the expression of ROS-related genes (primarily genes with antioxidant activity) when quantified immediately after MF exposure, suggesting a response to a small increase in ROS level. The possible upregulation of ROS-related genes is supported by the finding that the level of menadione-induced ROS was consistently decreased by 50 Hz MFs (not significantly by 60 Hz MFs) in several measurements 30 - 60 min after MF exposure. MF exposures did not affect cytosolic O2•- levels, DNA damage, or its repair rate. Changes in the expression of DNA damage-signaling genes in the MF- exposed cells did not exceed the expected rate of false positive findings. No firm evidence was found for differential effects from 50 Hz vs. 60 Hz MFs. Conclusions: While only weak effects were found on the endpoints measured, the results are consistent with MF effects on ROS signaling. pubmed.ncbi.nlm.nih.gov

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AI evidence extraction

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Study typein_vitro

Effect directionmixed

PopulationHuman SH-SY5Y neuroblastoma cells

Sample sizeNot supplied

ExposureELF · 24 h (with additional 1 h menadione treatment; ROS measured 30–60 min after MF exposure in some measurements)

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

After 24 h exposure to 100 µTRMS 50/60 Hz magnetic fields, there was suggestive evidence of a low-magnitude increase in expression of ROS-related genes immediately after exposure. Menadione-induced ROS was consistently decreased by 50 Hz magnetic fields (not significantly by 60 Hz) in several measurements 30–60 min after exposure. Magnetic field exposures did not affect cytosolic O2•- levels, DNA damage, or DNA repair rate, and changes in DNA damage-signaling gene expression did not exceed expected false positives; no firm evidence for differential effects between 50 Hz and 60 Hz was found.

Outcomes measured

Reactive oxygen species (ROS) production
Cytosolic superoxide anion (O2•-) levels
DNA damage (comet assay)
DNA damage repair rate
Gene expression related to oxidative stress
Gene expression related to DNA damage signaling

Limitations

Sample size not reported in abstract
Effects described as weak/suggestive and low-magnitude
Some findings (e.g., 60 Hz effects on menadione-induced ROS) reported as not significant
Potential for false positive gene expression findings noted by authors

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "24 h (with additional 1 h menadione treatment; ROS measured 30–60 min after MF exposure in some measurements)"
  },
  "population": "Human SH-SY5Y neuroblastoma cells",
  "sample_size": null,
  "outcomes": [
    "Reactive oxygen species (ROS) production",
    "Cytosolic superoxide anion (O2•-) levels",
    "DNA damage (comet assay)",
    "DNA damage repair rate",
    "Gene expression related to oxidative stress",
    "Gene expression related to DNA damage signaling"
  ],
  "main_findings": "After 24 h exposure to 100 µTRMS 50/60 Hz magnetic fields, there was suggestive evidence of a low-magnitude increase in expression of ROS-related genes immediately after exposure. Menadione-induced ROS was consistently decreased by 50 Hz magnetic fields (not significantly by 60 Hz) in several measurements 30–60 min after exposure. Magnetic field exposures did not affect cytosolic O2•- levels, DNA damage, or DNA repair rate, and changes in DNA damage-signaling gene expression did not exceed expected false positives; no firm evidence for differential effects between 50 Hz and 60 Hz was found.",
  "effect_direction": "mixed",
  "limitations": [
    "Sample size not reported in abstract",
    "Effects described as weak/suggestive and low-magnitude",
    "Some findings (e.g., 60 Hz effects on menadione-induced ROS) reported as not significant",
    "Potential for false positive gene expression findings noted by authors"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "50 Hz",
    "60 Hz",
    "extremely low frequency",
    "magnetic fields",
    "SH-SY5Y",
    "neuroblastoma cells",
    "ROS",
    "oxidative stress",
    "DNA damage",
    "comet assay",
    "RT-qPCR",
    "menadione",
    "DNA repair"
  ],
  "suggested_hubs": [
    {
      "slug": "elf-magnetic-fields",
      "weight": 0.95,
      "reason": "In vitro study of 50/60 Hz magnetic field exposure and oxidative/DNA damage endpoints."
    }
  ]
}

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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: 10.1080/09553002.2022.2055803
PubMed: 35320060

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