Effects of Mobile Phone EMF on β-Amyloid-Induced Oxidative Stress in Human and Rat Primary Astrocytes

2019 · Benefit · Low evidence

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BenefitLow evidencePaper 1834

Study snapshot

Publicationmanual · 2019

Study typein_vitro

Reported directionBenefit

Evidence ratingLow

Abstract

Effects of Mobile Phone EMF on β-Amyloid-Induced Oxidative Stress in Human and Rat Primary Astrocytes Tsoy A, Saliev T, Abzhanova E, Turgambayeva A, Kaiyrlykyzy A, Akishev M, Saparbayev S, Umbayev B, Askarova S. The Effects of Mobile Phone Radiofrequency Electromagnetic Fields on β-Amyloid-Induced Oxidative Stress in Human and Rat Primary Astrocytes. Neuroscience. Published online Apr 3, 2019. doi.org Highlights • EMF of 918 MHz decreases Aß42- induced cellular and mitochondrial ROS in human and rat primary astrocytes. • EMF of 918 MHz increases mitochondrial membrane potential in rat primary astrocytes. • EMF of 918 MHz suppresses induced by Aß42 activation of NADPH oxidase in rat primary astrocytes. • EMF of 918 MHz suppresses H2O2-induced phosphorylation of p38MAPK and ERK 1/2 in rat primary astrocytes. Abstract Amyloid beta peptide (Aβ) is implicated in the development of pathological reactions associated with Alzheimer's disease (AD), such as oxidative stress, neuro-inflammation and death of brain cells. Current pharmacological approaches to treat AD are not able to control the deposition of Aβ and suppression of Aβ- induced cellular response. There is a growing body of evidence that exposure to radiofrequency electromagnetic field (RF-EMF) causes a decrease of beta-amyloid deposition in the brains and provides cognitive benefits to Alzheimer's Tg mice. Herein, we investigated the effects of mobile phone radiofrequency EMF of 918 MHz on reactive oxygen species (ROS) formation, mitochondrial membrane potential (MMP), activity of NADPH-oxidase, and phosphorylation of p38MAPK and ERK1/2 kinases in human and rat primary astrocytes in the presence of Aβ42 and H2O2. Our data demonstrate that EMF is able to reduce Aβ42- and H2O2-induced cellular ROS, abrogate Aβ₄₂-induced production of mitochondrial ROS and the co-localization between the cytosolic (p47- phox) and membrane (gp91-phox) subunits of NADPH oxidase, while increasing MMP, and inhibiting H2O2- induced phosphorylation of p38MAPK and ERK1/2 in primary astrocytes. Yet, EMF was not able to modulate alterations in the phosphorylation state of the MAPKs triggered by Aβ42. Our findings provide an insight into the mechanisms of cellular and molecular responses of astrocytes on RF-EMF exposure and indicate the therapeutic potential of RF-EMF for the treatment of Alzheimer's disease. Excerpt In summary, our data showed that EMF treatment of brain cells with parameters similar to irradiation from the ordinary mobile phone (918 MHz; GSM) was capable of suppressing oxidative stress triggered by Aβ42 and H2O2, thus indicating its possible therapeutic benefit. Our data conform to the previous reports on beneficial impact of EMF that can be employed for the treatment of neurodegenerative disorders such as Alzheimer's disease. However, further studies are needed to validate the effectiveness and safety of EMF application in AD patients. sciencedirect.com

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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 directionbenefit

PopulationHuman and rat primary astrocytes

Sample sizeNot supplied

ExposureRF · 918 MHz

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

In human and rat primary astrocytes exposed to 918 MHz RF-EMF, EMF reduced Aβ42- and H2O2-induced cellular ROS and reduced Aβ42-induced mitochondrial ROS. In rat primary astrocytes, EMF increased mitochondrial membrane potential, suppressed Aβ42-associated NADPH oxidase subunit co-localization, and inhibited H2O2-induced phosphorylation of p38MAPK and ERK1/2; EMF did not modulate Aβ42-triggered MAPK phosphorylation changes.

Outcomes measured

Cellular reactive oxygen species (ROS)
Mitochondrial ROS
Mitochondrial membrane potential (MMP)
NADPH oxidase activity/co-localization of p47-phox and gp91-phox subunits
Phosphorylation of p38MAPK
Phosphorylation of ERK1/2

Limitations

Exposure parameters beyond frequency (e.g., SAR, duration) not reported in the provided abstract/metadata
In vitro model (primary astrocytes) may not generalize to in vivo or clinical outcomes
Some signaling outcomes were not affected (e.g., Aβ42-triggered MAPK phosphorylation not modulated)

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": "mobile phone",
    "frequency_mhz": 918,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human and rat primary astrocytes",
  "sample_size": null,
  "outcomes": [
    "Cellular reactive oxygen species (ROS)",
    "Mitochondrial ROS",
    "Mitochondrial membrane potential (MMP)",
    "NADPH oxidase activity/co-localization of p47-phox and gp91-phox subunits",
    "Phosphorylation of p38MAPK",
    "Phosphorylation of ERK1/2"
  ],
  "main_findings": "In human and rat primary astrocytes exposed to 918 MHz RF-EMF, EMF reduced Aβ42- and H2O2-induced cellular ROS and reduced Aβ42-induced mitochondrial ROS. In rat primary astrocytes, EMF increased mitochondrial membrane potential, suppressed Aβ42-associated NADPH oxidase subunit co-localization, and inhibited H2O2-induced phosphorylation of p38MAPK and ERK1/2; EMF did not modulate Aβ42-triggered MAPK phosphorylation changes.",
  "effect_direction": "benefit",
  "limitations": [
    "Exposure parameters beyond frequency (e.g., SAR, duration) not reported in the provided abstract/metadata",
    "In vitro model (primary astrocytes) may not generalize to in vivo or clinical outcomes",
    "Some signaling outcomes were not affected (e.g., Aβ42-triggered MAPK phosphorylation not modulated)"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "radiofrequency electromagnetic field",
    "RF-EMF",
    "mobile phone",
    "918 MHz",
    "GSM",
    "astrocytes",
    "amyloid beta",
    "Aβ42",
    "oxidative stress",
    "reactive oxygen species",
    "mitochondrial membrane potential",
    "NADPH oxidase",
    "p38MAPK",
    "ERK1/2",
    "Alzheimer's disease"
  ],
  "suggested_hubs": [
    {
      "slug": "mobile-phones-rf",
      "weight": 0.9,
      "reason": "Study tests mobile phone-like RF-EMF exposure at 918 MHz (GSM)."
    },
    {
      "slug": "alzheimer-neurodegeneration",
      "weight": 0.75,
      "reason": "Outcomes are framed around Aβ42-induced oxidative stress and potential relevance to Alzheimer's disease."
    }
  ]
}

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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.neuroscience.2019.03.058
PubMed: Not supplied

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