Oxidative stress and prevention of the adaptive response to chronic iron overload in the brain of young adult rats exposed to a 150 kilohertz electromagnetic field.

Neuroscience · 2011 · Harm · Low evidence

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HarmLow evidencePaper 4466

Chronic iron overload stimulated antioxidant defenses without causing oxidative stress. EMF exposure at 150 kHz increased lipid peroxidation without affecting antioxidant defenses. Combined EMF and iron overload increased lipid peroxidation further and abolis…

Study snapshot

PublicationNeuroscience · 2011

Study typeanimal

Reported directionHarm

Evidence ratingLow

Abstract

Iron surcharge may induce an oxidative stress-based decline in several neurological functions. In addition, electromagnetic fields (EMF) of frequencies up to about 100 kHz, emitted by electric/electronic devices, have been suggested to enhance free radical production through an iron dependent pathway. The purpose of this study was therefore to determine a possible relationship between iron status, exposure to EMF, and brain oxidative stress in young adult rats. Samples were micro-dissected from prefrontal cortex, hippocampus, striatum, and cerebellum after chronic saline or iron overload (IO) as well as after chronic sham exposure or exposure to a 150 kHz EMF or after combining EMF exposure with IO. The brain samples were used to monitor oxidative stress-induced lipid peroxidation and activity of the antioxidant enzymes superoxide dismutase and catalase. While IO did not induce any oxidative stress in young adult rats, it stimulated antioxidant defenses in the cerebellum and prefrontal cortex in particular. On the contrary, EMF exposure stimulated lipid peroxidation mainly in the cerebellum, without affecting antioxidant defenses. When EMF was coapplied with IO, lipid peroxidation was further increased as compared to EMF alone while the increase in antioxidant defenses triggered by the sole IO was abolished. These data suggest that EMF exposure may be harmful in young adults by impairing the antioxidant defenses directed at preventing iron-induced oxidative stress.

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

Populationyoung adult rats

Sample sizeNot supplied

ExposurekHz · 0.15 MHz · chronic

Evidence strengthLowConfidence: 40% · Peer reviewed: yes

Main findings

Outcomes measured

oxidative stress-induced lipid peroxidation
activity of antioxidant enzymes superoxide dismutase and catalase

Limitations

animal study, results may not directly translate to humans
sample size not specified
specific absorption rate (SAR) not reported

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "kHz",
    "source": null,
    "frequency_mhz": 0.15,
    "sar_wkg": null,
    "duration": "chronic"
  },
  "population": "young adult rats",
  "sample_size": null,
  "outcomes": [
    "oxidative stress-induced lipid peroxidation",
    "activity of antioxidant enzymes superoxide dismutase and catalase"
  ],
  "main_findings": "Chronic iron overload stimulated antioxidant defenses without causing oxidative stress. EMF exposure at 150 kHz increased lipid peroxidation without affecting antioxidant defenses. Combined EMF and iron overload increased lipid peroxidation further and abolished the antioxidant defense increase induced by iron overload alone.",
  "effect_direction": "harm",
  "limitations": [
    "animal study, results may not directly translate to humans",
    "sample size not specified",
    "specific absorption rate (SAR) not reported"
  ],
  "evidence_strength": "low",
  "confidence": 0.4,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "oxidative stress",
    "iron overload",
    "electromagnetic field",
    "150 kHz",
    "lipid peroxidation",
    "antioxidant enzymes",
    "brain",
    "rats"
  ],
  "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.neuroscience.2011.04.003
PubMed: 21497179

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