Exposure to 50Hz-sinusoidal electromagnetic field induces DNA damage-independent autophagy.

The international journal of biochemistry & cell biology · 2016 · Mixed · Low evidence

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MixedLow evidencePaper 4859

Study snapshot

PublicationThe international journal of biochemistry & cell biology · 2016

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

As electromagnetic field (EMF) is commonly encountered within our daily lives, the biological effects of EMF are of great concern. Autophagy is a key process for maintaining cellular homeostasis, and it can also reveal cellular responses to environmental stimuli. In this study, we aim to investigate the biological effects of a 50Hz-sinusoidal electromagnetic field on autophagy and we identified its mechanism of action in Chinese Hamster Lung (CHL) cells. CHL cells were exposed to a 50Hz sinusoidal EMF at 0.4mT for 30min or 24h. In this study, we found that a 0.4mT EMF resulted in: (i) an increase in LC3-II expression and increased autophagosome formation; (ii) no significant difference in the incidence of γH2AX foci between the sham and exposure groups; (iii) reorganized actin filaments and increased pseudopodial extensions without promoting cell migration; and (iv) enhanced cell apoptosis when autophagy was blocked by Bafilomycin A1. These results implied that DNA damage was not directly involved in the autophagy induced by a 0.4mT 50Hz EMF. In addition, an EMF induced autophagy balanced the cellular homeostasis to protect the cells from severe adverse biological consequences.

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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 directionmixed

PopulationChinese Hamster Lung (CHL) cells

Sample sizeNot supplied

ExposureELF · 0.05 MHz · 30 min or 24 h

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

CHL cells exposed to a 50 Hz sinusoidal EMF (0.4 mT) for 30 min or 24 h showed increased LC3-II expression and autophagosome formation. There was no significant difference in γH2AX foci between sham and exposed groups, and actin filaments were reorganized with increased pseudopodial extensions without promoting cell migration; apoptosis was enhanced when autophagy was blocked by Bafilomycin A1.

Outcomes measured

Autophagy (LC3-II expression, autophagosome formation)
DNA damage marker (γH2AX foci)
Actin filament organization and pseudopodial extensions
Cell migration
Apoptosis when autophagy blocked (Bafilomycin A1)

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": null,
    "frequency_mhz": 0.05,
    "sar_wkg": null,
    "duration": "30 min or 24 h"
  },
  "population": "Chinese Hamster Lung (CHL) cells",
  "sample_size": null,
  "outcomes": [
    "Autophagy (LC3-II expression, autophagosome formation)",
    "DNA damage marker (γH2AX foci)",
    "Actin filament organization and pseudopodial extensions",
    "Cell migration",
    "Apoptosis when autophagy blocked (Bafilomycin A1)"
  ],
  "main_findings": "CHL cells exposed to a 50 Hz sinusoidal EMF (0.4 mT) for 30 min or 24 h showed increased LC3-II expression and autophagosome formation. There was no significant difference in γH2AX foci between sham and exposed groups, and actin filaments were reorganized with increased pseudopodial extensions without promoting cell migration; apoptosis was enhanced when autophagy was blocked by Bafilomycin A1.",
  "effect_direction": "mixed",
  "limitations": [],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "50 Hz",
    "ELF-EMF",
    "0.4 mT",
    "autophagy",
    "LC3-II",
    "autophagosome",
    "γH2AX",
    "actin cytoskeleton",
    "apoptosis",
    "Bafilomycin A1",
    "Chinese Hamster Lung cells"
  ],
  "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: 10.1016/j.biocel.2016.05.009
PubMed: 27177844

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