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Cell phone exposure induces apoptosis, mitochondrial oxidative stress & TRPV1 channel activation in hippocampus of rats

2018 · Harm · Low evidence

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HarmLow evidencePaper 2172

Rats exposed long-term to 900 or 1800 MHz EMR showed increased TRPV1 currents, Ca2+ influx, ROS production, mitochondrial membrane depolarization, apoptosis, and caspase-3/9 activities in hippocampus and dorsal root ganglion compared with controls. Effects we…

Study snapshot

Publicationmanual · 2018
Study typeanimal
Reported directionHarm
Evidence ratingLow

Abstract

Cell phone exposure induces apoptosis, mitochondrial oxidative stress & TRPV1 channel activation in hippocampus of rats Ertilav K, Uslusoy F, Ataizi S, Nazıroğlu M. Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats. Metab Brain Dis. 2018 Jan 13. doi: 10.1007/s11011-017-0180-4. Abstract Mobile phone providers use electromagnetic radiation (EMR) with frequencies ranging from 900 to 1800 MHz. The increasing use of mobile phones has been accompanied by several potentially pathological consequences, such as neurological diseases related to hippocampal (HIPPON) and dorsal root ganglion neuron (DRGN). The TRPV1 channel is activated different stimuli, including CapN, high temperature and oxidative stress. We investigated the contribution TRPV1 to mitochondrial oxidative stress and apoptosis in HIPPON and DRGN following long term exposure to 900 and 1800 MHz in a rat model. Twenty-four adult rats were equally divided into the following groups: (1) control, (2) 900 MHz, and (3) 1800 MHz exposure. Each experimental group was exposed to EMR for 60 min/ 5 days of the week during the one year. The 900 and 1800 MHz EMR exposure induced increases in TRPV1 currents, intracellular free calcium influx (Ca2+), reactive oxygen species (ROS) production, mitochondrial membrane depolarization (JC-1), apoptosis, and caspase 3 and 9 activities in the HIPPON and DRGN. These deleterious processes were further increased in the 1800 MHz experimental group compared to the 900 MHz exposure group. In conclusion, mitochondrial oxidative stress, programmed cell death and Ca2+ entry pathway through TRPV1 activation in the HIPPON and DRGN of rats were increased in the rat model following exposure to 900 and 1800 MHz cell frequencies. Our results suggest that exposure to 900 and 1800 MHz EMR may induce a dose-associated, TRPV1-mediated stress response. ncbi.nlm.nih.gov

Machine Enhanced Logic

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 typeanimal
Effect directionharm
PopulationAdult rats
Sample size24
ExposureRF · 60 min/day, 5 days/week, for 1 year
Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Rats exposed long-term to 900 or 1800 MHz EMR showed increased TRPV1 currents, Ca2+ influx, ROS production, mitochondrial membrane depolarization, apoptosis, and caspase-3/9 activities in hippocampus and dorsal root ganglion compared with controls. Effects were reported as greater in the 1800 MHz group than the 900 MHz group.

Outcomes measured

  • TRPV1 currents/activation
  • Intracellular Ca2+ influx
  • Reactive oxygen species (ROS) production
  • Mitochondrial membrane depolarization (JC-1)
  • Apoptosis
  • Caspase-3 activity
  • Caspase-9 activity

Limitations

  • Specific SAR or exposure intensity not reported in the abstract
  • Animal model; generalizability to humans is uncertain
  • Mechanistic outcomes only; no behavioral/clinical endpoints described in the abstract
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": "mobile phone",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "60 min/day, 5 days/week, for 1 year"
  },
  "population": "Adult rats",
  "sample_size": 24,
  "outcomes": [
    "TRPV1 currents/activation",
    "Intracellular Ca2+ influx",
    "Reactive oxygen species (ROS) production",
    "Mitochondrial membrane depolarization (JC-1)",
    "Apoptosis",
    "Caspase-3 activity",
    "Caspase-9 activity"
  ],
  "main_findings": "Rats exposed long-term to 900 or 1800 MHz EMR showed increased TRPV1 currents, Ca2+ influx, ROS production, mitochondrial membrane depolarization, apoptosis, and caspase-3/9 activities in hippocampus and dorsal root ganglion compared with controls. Effects were reported as greater in the 1800 MHz group than the 900 MHz group.",
  "effect_direction": "harm",
  "limitations": [
    "Specific SAR or exposure intensity not reported in the abstract",
    "Animal model; generalizability to humans is uncertain",
    "Mechanistic outcomes only; no behavioral/clinical endpoints described in the abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "mobile phone",
    "900 MHz",
    "1800 MHz",
    "rats",
    "hippocampus",
    "dorsal root ganglion",
    "TRPV1",
    "oxidative stress",
    "mitochondria",
    "apoptosis",
    "caspase-3",
    "caspase-9",
    "ROS",
    "calcium influx"
  ],
  "suggested_hubs": [
    {
      "slug": "mobile-phones-rf",
      "weight": 0.9,
      "reason": "Study examines long-term exposure to cell phone frequencies (900/1800 MHz) and biological effects in rats."
    }
  ]
}
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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: 10.1007/s11011-017-0180-4
PubMed: Not supplied

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