Impact of 2.45 GHz microwave radiation on the testicular inflammatory pathway biomarkers in young rats: The role of gallic acid.

Environmental toxicology · 2016 · Harm · Low evidence

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HarmLow evidencePaper 6573

Study snapshot

PublicationEnvironmental toxicology · 2016

Study typeanimal

Reported directionHarm

Evidence ratingLow

Abstract

The aim of this study was to investigate electromagnetic radiation (EMR) transmitted by wireless devices (2.45 GHz), which may cause physiopathological or ultrastructural changes, in the testes of rats. We addressed if the supplemental gallic acid (GA) may reduce these adverse effects. Six-week-old male Sprague Dawley rats were used in this study. Forty eight rats were equally divided into four groups, which were named: Sham, EMR only (EMR, 3 h day for 30 days), EMR + GA (30 mg/kg/daily), and GA (30 mg/kg/daily) groups. Malondialdehyde (MDA) and total oxidant status (TOS) levels increased (p = 0.001 for both) in EMR only group. TOS and oxidative stress index (OSI) levels decreased in GA treated group significantly (p = 0.001 and p = 0.045, respectively). Total antioxidant status (TAS) activities decreased in EMR only group and increased in GA treatment group (p = 0.001 and p = 0.029, respectively). Testosterone and vascular endothelial growth factor (VEGF) levels decreased in EMR only group, but this was not statistically significant. Testosterone and VEGF levels increased in EMR+GA group, compared with EMR only group (p = 0.002), and also increased in GA group compared with the control and EMR only group (p = 0.044 and p = 0.032, respectively). Prostaglandin E (PGE ) and calcitonin gene releated peptide (CGRP) staining increased in tubules of the testes in EMR only group (p < 0.001 for both) and decreased in tubules of the testes in EMR+GA group (p < 0.001 for all parameters). In EMR only group, most of the tubules contained less spermatozoa, and the spermatozoon counts decreased in tubules of the testes. All these findings and the regenerative reaction, characterized by mitotic activity, increased in seminiferous tubules cells of the testes in EMR+GA group (p < 0.001). Long term EMR exposure resulted in testicular physiopathology via oxidative damage and inflammation. GA may have ameliorative effects on the prepubertal rat testes physiopathology. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1771-1784, 2016.

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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

PopulationSix-week-old male Sprague Dawley rats (young/prepubertal)

Sample size48

Exposuremicrowave · 2450 MHz · 3 h/day for 30 days

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Compared with sham, the EMR-only group showed increased oxidative stress markers (MDA and TOS; TAS decreased) and increased PGE and CGRP staining in testicular tubules, with fewer spermatozoa and decreased spermatozoon counts. Gallic acid co-treatment (EMR+GA) was associated with lower oxidative stress/inflammatory staining than EMR-only and with increased testosterone/VEGF versus EMR-only; histologic findings were described as improved with increased mitotic activity.

Outcomes measured

Testicular oxidative stress biomarkers (MDA, TOS, OSI, TAS)
Testosterone
Vascular endothelial growth factor (VEGF)
Inflammatory pathway biomarkers/staining (PGE, CGRP)
Testicular histology/physiopathology (seminiferous tubules, spermatozoa counts, mitotic activity/regenerative reaction)

Limitations

No SAR or dosimetry details reported in the abstract
Testosterone and VEGF decreases in EMR-only group were not statistically significant
Animal model; generalizability to humans not addressed in abstract

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "microwave",
    "source": "wireless devices",
    "frequency_mhz": 2450,
    "sar_wkg": null,
    "duration": "3 h/day for 30 days"
  },
  "population": "Six-week-old male Sprague Dawley rats (young/prepubertal)",
  "sample_size": 48,
  "outcomes": [
    "Testicular oxidative stress biomarkers (MDA, TOS, OSI, TAS)",
    "Testosterone",
    "Vascular endothelial growth factor (VEGF)",
    "Inflammatory pathway biomarkers/staining (PGE, CGRP)",
    "Testicular histology/physiopathology (seminiferous tubules, spermatozoa counts, mitotic activity/regenerative reaction)"
  ],
  "main_findings": "Compared with sham, the EMR-only group showed increased oxidative stress markers (MDA and TOS; TAS decreased) and increased PGE and CGRP staining in testicular tubules, with fewer spermatozoa and decreased spermatozoon counts. Gallic acid co-treatment (EMR+GA) was associated with lower oxidative stress/inflammatory staining than EMR-only and with increased testosterone/VEGF versus EMR-only; histologic findings were described as improved with increased mitotic activity.",
  "effect_direction": "harm",
  "limitations": [
    "No SAR or dosimetry details reported in the abstract",
    "Testosterone and VEGF decreases in EMR-only group were not statistically significant",
    "Animal model; generalizability to humans not addressed in abstract"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "2.45 GHz",
    "microwave radiation",
    "wireless devices",
    "testis",
    "oxidative stress",
    "inflammation",
    "malondialdehyde",
    "total oxidant status",
    "total antioxidant status",
    "testosterone",
    "VEGF",
    "PGE",
    "CGRP",
    "gallic acid",
    "Sprague Dawley rats"
  ],
  "suggested_hubs": [
    {
      "slug": "school-wi-fi",
      "weight": 0.35,
      "reason": "Exposure frequency (2.45 GHz) overlaps with Wi‑Fi band; study framed as wireless-device EMR."
    }
  ]
}

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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: 10.1002/tox.22179
PubMed: 26268881

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