Disordered redox metabolism of brain cells in rats exposed to low doses of ionizing radiation or UHF electromagnetic radiation.

Experimental oncology · 2016 · Harm · Low evidence

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HarmLow evidencePaper 2902

Compared with controls, rats exposed to ionizing radiation or non-thermal UHF EMR showed decreased ubisemiquinone in brain tissue (3-fold and 1.8-fold decreases, respectively) and significantly increased NO-FeS-protein complexes. Superoxide radical generation…

Study snapshot

PublicationExperimental oncology · 2016
Study typeanimal
Reported directionHarm
Evidence ratingLow

Abstract

AIM: To investigate the changes of redox-state of mammalian brain cells as the critical factor of initiation and formation of radiation damage of biological structures in setting of continuous exposure to low doses of ionizing radiation or fractionated ultra high frequency electromagnetic radiation (UHF EMR) at non-thermal levels. MATERIALS AND METHODS: The influence of low-intensity ionizing radiation was studied on outbred female rats kept for 1.5 years in the Chernobyl accident zone. The effects of total EMR in the UHF band of non-thermal spectrum were investigated on Wistar rats. The rate of formation of superoxide radicals and the rate of NO synthesis in mitochondria were determined by the EPR. RESULTS: After exposure to ionizing or UHF radiation, the levels of ubisemiquinone in brain tissue of rats decreased by 3 and 1.8 times, respectively. The content of NO-FeS-protein complexes in both groups increased significantly (р < 0.05). In the conditions of ionizing or EMR the rates of superoxide radical generation in electron-transport chain of brain cell mitochondria increased by 1.5- and 2-fold, respectively (р < 0.05). In brain tissue of rats kept in the Chernobyl zone, significant increase of NO content was registered; similar effect was observed in rats treated with UHFR (р < 0.05). CONCLUSIONS: The detected changes in the electron transport chain of mitochondria of brain cells upon low-intensity irradiation or UHF EMR cause the metabolic reprogramming of cell mitochondria that increases the rate of superoxide radical generation and nitric oxide, which may initiate the development of neurodegenerative diseases and cancer. This article is part of a Special Issue entitled "The Chornobyl Nuclear Accident: Thirty Years After".

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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
PopulationRats (outbred female rats; Wistar rats)
Sample sizeNot supplied
ExposureRF · fractionated UHF EMR (non-thermal levels); ionizing radiation exposure for 1.5 years in Chernobyl accident zone (separate group)
Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

Compared with controls, rats exposed to ionizing radiation or non-thermal UHF EMR showed decreased ubisemiquinone in brain tissue (3-fold and 1.8-fold decreases, respectively) and significantly increased NO-FeS-protein complexes. Superoxide radical generation rates in brain mitochondria increased (1.5-fold with ionizing radiation; 2-fold with UHF EMR; p<0.05), and NO content increased in both exposure groups (p<0.05).

Outcomes measured

  • Brain tissue ubisemiquinone levels
  • NO-FeS-protein complexes in brain tissue
  • Mitochondrial superoxide radical generation rate (electron transport chain)
  • Mitochondrial nitric oxide (NO) synthesis/content

Limitations

  • No sample size reported in abstract
  • UHF EMR exposure parameters (frequency, power density/SAR, schedule) not specified in abstract
  • Control/sham conditions not described in abstract
  • Two different rat strains and exposure paradigms used (Chernobyl-zone chronic exposure vs fractionated UHF EMR), limiting direct comparability
View raw extracted JSON
{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "fractionated UHF EMR (non-thermal levels); ionizing radiation exposure for 1.5 years in Chernobyl accident zone (separate group)"
  },
  "population": "Rats (outbred female rats; Wistar rats)",
  "sample_size": null,
  "outcomes": [
    "Brain tissue ubisemiquinone levels",
    "NO-FeS-protein complexes in brain tissue",
    "Mitochondrial superoxide radical generation rate (electron transport chain)",
    "Mitochondrial nitric oxide (NO) synthesis/content"
  ],
  "main_findings": "Compared with controls, rats exposed to ionizing radiation or non-thermal UHF EMR showed decreased ubisemiquinone in brain tissue (3-fold and 1.8-fold decreases, respectively) and significantly increased NO-FeS-protein complexes. Superoxide radical generation rates in brain mitochondria increased (1.5-fold with ionizing radiation; 2-fold with UHF EMR; p<0.05), and NO content increased in both exposure groups (p<0.05).",
  "effect_direction": "harm",
  "limitations": [
    "No sample size reported in abstract",
    "UHF EMR exposure parameters (frequency, power density/SAR, schedule) not specified in abstract",
    "Control/sham conditions not described in abstract",
    "Two different rat strains and exposure paradigms used (Chernobyl-zone chronic exposure vs fractionated UHF EMR), limiting direct comparability"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "UHF",
    "RF EMR",
    "non-thermal exposure",
    "rats",
    "brain",
    "mitochondria",
    "redox state",
    "oxidative stress",
    "superoxide",
    "nitric oxide",
    "EPR",
    "Chernobyl",
    "ionizing radiation"
  ],
  "suggested_hubs": [
    {
      "slug": "animal-studies",
      "weight": 0.9,
      "reason": "Experimental study in rats assessing brain mitochondrial/redox outcomes after UHF EMR exposure."
    }
  ]
}
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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: Not supplied
PubMed: 28230822

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