Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats

Metab Brain Dis · 2014 · Harm · Low evidence

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HarmLow evidencePaper 2741

Study snapshot

PublicationMetab Brain Dis · 2014

Study typeanimal

Reported directionHarm

Evidence ratingLow

Abstract

Incidence rates of epilepsy and use of Wi-Fi worldwide have been increasing. TRPV1 is a Ca(2+) permeable and non-selective channel, gated by noxious heat, oxidative stress and capsaicin (CAP). The hyperthermia and oxidant effects of Wi-Fi may induce apoptosis and Ca(2+) entry through activation of TRPV1 channel in epilepsy. Therefore, we tested the effects of Wi-Fi (2.45 GHz) exposure on Ca(2+) influx, oxidative stress and apoptosis through TRPV1 channel in the murine dorsal root ganglion (DRG) and hippocampus of pentylentetrazol (PTZ)-induced epileptic rats. Rats in the present study were divided into two groups as controls and PTZ. The PTZ groups were divided into two subgroups namely PTZ + Wi-Fi and PTZ + Wi-Fi + capsazepine (CPZ). The hippocampal and DRG neurons were freshly isolated from the rats. The DRG and hippocampus in PTZ + Wi-Fi and PTZ + Wi-Fi + CPZ groups were exposed to Wi-Fi for 1 hour before CAP stimulation. The cytosolic free Ca(2+), reactive oxygen species production, apoptosis, mitochondrial membrane depolarization, caspase-3 and -9 values in hippocampus were higher in the PTZ group than in the control although cell viability values decreased. The Wi-Fi exposure induced additional effects on the cytosolic Ca(2+) increase. However, pretreatment of the neurons with CPZ, results in a protection against epilepsy-induced Ca(2+) influx, apoptosis and oxidative damages. In results of whole cell patch-clamp experiments, treatment of DRG with Ca(2+) channel antagonists [thapsigargin, verapamil + diltiazem, 2-APB, MK-801] indicated that Wi-Fi exposure induced Ca(2+) influx via the TRPV1 channels. In conclusion, epilepsy and Wi-Fi in our experimental model is involved in Ca(2+) influx and oxidative stress-induced hippocampal and DRG death through activation of TRPV1 channels, and negative modulation of this channel activity by CPZ pretreatment may account for the neuroprotective activity against oxidative stress.

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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 typeanimal

Effect directionharm

PopulationPTZ-induced epileptic rats; hippocampal and dorsal root ganglion (DRG) neurons freshly isolated

Sample sizeNot supplied

ExposureRF · 2450 MHz · 1 hour

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

In hippocampal and DRG neurons from PTZ-induced epileptic rats, Wi‑Fi (2.45 GHz) exposure for 1 hour before capsaicin stimulation was reported to induce additional increases in cytosolic Ca(2+). Patch-clamp experiments with pharmacologic antagonists were interpreted as indicating Wi‑Fi exposure induced Ca(2+) influx via TRPV1 channels, and capsazepine pretreatment was reported to protect against epilepsy-associated Ca(2+) influx, apoptosis, and oxidative damage.

Outcomes measured

Cytosolic free Ca(2+)
Reactive oxygen species (oxidative stress)
Apoptosis
Mitochondrial membrane depolarization
Caspase-3
Caspase-9
Cell viability
Whole-cell patch-clamp measures of Ca(2+) influx/TRPV1 involvement

Limitations

Sample size not reported in abstract
Exposure metric (e.g., SAR/power density) not reported in abstract
Wi‑Fi exposure appears applied to isolated tissues/neurons ex vivo rather than whole-animal exposure (as described)
Findings are from an animal model (PTZ-induced epilepsy) and may not generalize to humans
Multiple pharmacologic manipulations; potential for confounding by experimental conditions not detailed in abstract

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": "wi-fi",
    "frequency_mhz": 2450,
    "sar_wkg": null,
    "duration": "1 hour"
  },
  "population": "PTZ-induced epileptic rats; hippocampal and dorsal root ganglion (DRG) neurons freshly isolated",
  "sample_size": null,
  "outcomes": [
    "Cytosolic free Ca(2+)",
    "Reactive oxygen species (oxidative stress)",
    "Apoptosis",
    "Mitochondrial membrane depolarization",
    "Caspase-3",
    "Caspase-9",
    "Cell viability",
    "Whole-cell patch-clamp measures of Ca(2+) influx/TRPV1 involvement"
  ],
  "main_findings": "In hippocampal and DRG neurons from PTZ-induced epileptic rats, Wi‑Fi (2.45 GHz) exposure for 1 hour before capsaicin stimulation was reported to induce additional increases in cytosolic Ca(2+). Patch-clamp experiments with pharmacologic antagonists were interpreted as indicating Wi‑Fi exposure induced Ca(2+) influx via TRPV1 channels, and capsazepine pretreatment was reported to protect against epilepsy-associated Ca(2+) influx, apoptosis, and oxidative damage.",
  "effect_direction": "harm",
  "limitations": [
    "Sample size not reported in abstract",
    "Exposure metric (e.g., SAR/power density) not reported in abstract",
    "Wi‑Fi exposure appears applied to isolated tissues/neurons ex vivo rather than whole-animal exposure (as described)",
    "Findings are from an animal model (PTZ-induced epilepsy) and may not generalize to humans",
    "Multiple pharmacologic manipulations; potential for confounding by experimental conditions not detailed in abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "Wi-Fi",
    "2.45 GHz",
    "RF-EMF",
    "epilepsy",
    "PTZ",
    "TRPV1",
    "capsaicin",
    "capsazepine",
    "calcium influx",
    "oxidative stress",
    "apoptosis",
    "hippocampus",
    "dorsal root ganglion",
    "patch-clamp"
  ],
  "suggested_hubs": [
    {
      "slug": "school-wi-fi",
      "weight": 0.6,
      "reason": "Study explicitly investigates Wi‑Fi (2.45 GHz) exposure effects."
    }
  ]
}

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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/s11011-014-9549-9
PubMed: 24792079

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