Hyperpolarization of plasma membrane of tumor cells sensitive to antiapoptotic effects of magnetic fields.
← Research streamStatic and extremely low-frequency (ELF) pulsating magnetic fields of different intensities altered plasma membrane potential. Magnetic fields induced plasma membrane hyperpolarization in cells sensitive to the antiapoptotic effect of magnetic fields, while i…
Study snapshot
Abstract
Chemical/physical agents able to prevent apoptosis are receiving much attention for their potential health hazard as tumor promoters. Magnetic fields (MFs), which have been shown to increase the occurrence of some tumors, reduce damage-induced apoptosis by a mechanism involving Ca2+ entry into cells. In order to discover the mechanism of such effect of MFs, we investigated the interference of MFs on cell metabolism and analyzed cell parameters that are involved in apoptotic signaling and regulation of Ca2+ fluxes. Here we show that different types (static and extremely low-frequency, ELF pulsating) of MFs of different intensities alter plasma membrane potential. Interestingly, MFs induce plasma membrane hyperpolarization in cells sensitive to the antiapoptotic effect of MFs, whereas cells that are insensitive showed a plasma membrane depolarization. These opposite effects suggest that protection against apoptosis and membrane potential modulation are correlated, plasma membrane hyperpolarization possibly being part of the signal transduction chain determining MFs' antiapoptotic effect.
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
Static and extremely low-frequency (ELF) pulsating magnetic fields of different intensities altered plasma membrane potential. Magnetic fields induced plasma membrane hyperpolarization in cells sensitive to the antiapoptotic effect of magnetic fields, while insensitive cells showed plasma membrane depolarization; the authors suggest these effects are correlated with protection against apoptosis.
Outcomes measured
- Apoptosis (damage-induced; antiapoptotic effects)
- Plasma membrane potential (hyperpolarization/depolarization)
- Ca2+ entry/fluxes (mechanistic involvement)
Limitations
- No specific magnetic field intensities reported in the abstract
- No exposure duration reported in the abstract
- Study design, model system (e.g., specific cell lines), and sample size not described in the abstract
View raw extracted JSON
{
"study_type": "other",
"exposure": {
"band": "ELF",
"source": "other",
"frequency_mhz": null,
"sar_wkg": null,
"duration": null
},
"population": null,
"sample_size": null,
"outcomes": [
"Apoptosis (damage-induced; antiapoptotic effects)",
"Plasma membrane potential (hyperpolarization/depolarization)",
"Ca2+ entry/fluxes (mechanistic involvement)"
],
"main_findings": "Static and extremely low-frequency (ELF) pulsating magnetic fields of different intensities altered plasma membrane potential. Magnetic fields induced plasma membrane hyperpolarization in cells sensitive to the antiapoptotic effect of magnetic fields, while insensitive cells showed plasma membrane depolarization; the authors suggest these effects are correlated with protection against apoptosis.",
"effect_direction": "mixed",
"limitations": [
"No specific magnetic field intensities reported in the abstract",
"No exposure duration reported in the abstract",
"Study design, model system (e.g., specific cell lines), and sample size not described in the abstract"
],
"evidence_strength": "insufficient",
"confidence": 0.66,
"peer_reviewed_likely": "yes",
"keywords": [
"magnetic fields",
"static magnetic field",
"ELF pulsating magnetic field",
"apoptosis",
"antiapoptotic effect",
"tumor cells",
"plasma membrane potential",
"hyperpolarization",
"depolarization",
"calcium entry"
],
"suggested_hubs": [
{
"slug": "mechanisms",
"weight": 0.78,
"reason": "Focuses on mechanistic links between magnetic fields, membrane potential changes, Ca2+ fluxes, and apoptosis."
}
]
}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: 10.1196/annals.1378.024
PubMed: 17384265
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