MAP kinase activation in cells exposed to a 60 Hz electromagnetic field.
← Research streamMAPK/ERK was activated in HL-60 human leukemia cells, MCF-7 human breast cancer cells, and rat fibroblast 3Y1 cells exposed to a 60 Hz, 1 Gauss electromagnetic field. The level of MAPK activation with EMF exposure was approximately equivalent to that seen wit…
Study snapshot
Abstract
This research provides evidence that mitogen-activated protein kinase or extracellular signal-regulated kinase (MAPK/ERK) is activated in HL-60 human leukemia cells, MCF-7 human breast cancer cells, and rat fibroblast 3Y1 cells exposed to a 60 Hertz (Hz), 1 Gauss (G) electromagnetic field (EMF). The effects of EMF exposure were compared to those observed using 12-O-tetradecanoylphorbal-13-acetate (TPA) treatment. The level of MAPK activation in cells exposed to EMF was approximately equivalent to that in cells treated with 0.1-0.5 ng/ml of TPA. A role for protein kinase C (PKC) in the process leading to MAPK activation in EMF exposed cells is also suggested by the results. MAPK activation is negated by an inhibitor to PKCalpha, but not PKCdelta inhibitors, in cells subjected to EMF exposure or TPA treatment. Thus, similarities between the effects of EMF exposure and TPA treatment are supported by this investigation. This provides a possible method for revealing other participants in EMF-cell interaction, since the TPA induction pathway is well documented.
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
MAPK/ERK was activated in HL-60 human leukemia cells, MCF-7 human breast cancer cells, and rat fibroblast 3Y1 cells exposed to a 60 Hz, 1 Gauss electromagnetic field. The level of MAPK activation with EMF exposure was approximately equivalent to that seen with 0.1–0.5 ng/ml TPA, and MAPK activation was negated by a PKCα inhibitor but not by PKCδ inhibitors in EMF-exposed or TPA-treated cells.
Outcomes measured
- MAPK/ERK activation
- PKC involvement in MAPK activation (PKCα vs PKCδ inhibitors)
- Comparison of EMF effects to TPA treatment
Limitations
- Exposure duration not reported in abstract
- Sample sizes and replication details not reported in abstract
- In vitro cell models; relevance to in vivo health outcomes not addressed in abstract
View raw extracted JSON
{
"study_type": "in_vitro",
"exposure": {
"band": "ELF",
"source": null,
"frequency_mhz": null,
"sar_wkg": null,
"duration": null
},
"population": null,
"sample_size": null,
"outcomes": [
"MAPK/ERK activation",
"PKC involvement in MAPK activation (PKCα vs PKCδ inhibitors)",
"Comparison of EMF effects to TPA treatment"
],
"main_findings": "MAPK/ERK was activated in HL-60 human leukemia cells, MCF-7 human breast cancer cells, and rat fibroblast 3Y1 cells exposed to a 60 Hz, 1 Gauss electromagnetic field. The level of MAPK activation with EMF exposure was approximately equivalent to that seen with 0.1–0.5 ng/ml TPA, and MAPK activation was negated by a PKCα inhibitor but not by PKCδ inhibitors in EMF-exposed or TPA-treated cells.",
"effect_direction": "mixed",
"limitations": [
"Exposure duration not reported in abstract",
"Sample sizes and replication details not reported in abstract",
"In vitro cell models; relevance to in vivo health outcomes not addressed in abstract"
],
"evidence_strength": "low",
"confidence": 0.78,
"peer_reviewed_likely": "yes",
"keywords": [
"ELF EMF",
"60 Hz",
"1 Gauss",
"MAPK",
"ERK",
"protein kinase C",
"PKCα",
"HL-60",
"MCF-7",
"3Y1 fibroblast",
"TPA"
],
"suggested_hubs": [
{
"slug": "occupational-exposure",
"weight": 0.35,
"reason": "Study involves 60 Hz ELF exposure, relevant to power-frequency environments (though source context not specified)."
}
]
}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: 10.1002/jcb.10704
PubMed: 14635193
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