Protective role of spermine against male reproductive aberrations induced by EMF exposure in the rat

2019 · Harm · Low evidence

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HarmLow evidencePaper 1817

Study snapshot

Publicationmanual · 2019

Study typeanimal

Reported directionHarm

Evidence ratingLow

Abstract

Protective role of spermine against male reproductive aberrations induced by EMF exposure in the rat Shahin NN, El-Nabarawy NA, Gouda AS, Megarbane B. The protective role of spermine against male reproductive aberrations induced by exposure to electromagnetic field - An experimental investigation in the rat. Toxicology and Applied Pharmacology. 370:117-130. May, 2019. DOI: 10.1016/j.taap.2019.03.009 Highlights • Exposure to electromagnetic field (EMF) impairs spermatogenesis and steroidogenesis. • EMF toxicity is mediated by oxidative, inflammatory, apoptotic and DNA perturbations. • Spermine exhibits protective effects against EMF-induced alteration in male fertility. • Protection is at least in part due to anti-oxidative and anti-apoptotic effects. Abstract The exponentially increasing use of electromagnetic field (EMF)-emitting devices imposes substantial health burden on modern societies with particular concerns of male infertility. Limited studies have addressed the modulation of this risk by protective agents. We investigated the hazardous effects of rat exposure to EMF (900 MHz, 2 h/day for 8 weeks) on male fertility and evaluated the possible protective effect of the polyamine, spermine, against EMF-induced alterations. Exposure to EMF significantly decreased sperm count, viability and motility, and increased sperm deformities. EMF-exposed rats exhibited significant reductions in serum inhibin B and testosterone along with elevated activin A, follicle-stimulating hormone, luteinizing hormone and estradiol concentrations. Testicular steroidogenic acute regulatory protein (StAR), c-kit mRNA expression and testicular activities of the key androgenic enzymes 3 beta- and 17 beta-hydroxysteroid dehydrogenases were significantly attenuated following exposure to EMF. Exposure led to testicular lipid peroxidation, decreased catalase and glutathione peroxidase activities and triggered nuclear factor-kappa B p65, inducible nitric oxide synthase, cyclooxygenase-2 and caspase-3 overexpression. EMF-exposed rats showed testicular DNA damage as indicated by elevated comet parameters. Spermine administration (2.5 mg/Kg/day intraperitoneally for 8 weeks) prevented EMF-induced alterations in the sperm and hormone profiles, StAR and c-kit expression and androgenic enzyme activities. Spermine hampered EMF-induced oxidative, inflammatory, apoptotic and DNA perturbations. Histological and histomorphometric analysis of the testes supported all biochemical findings. In conclusion, rat exposure to EMF disrupts sperm and hormone profiles with underlying impairment of steroidogenesis and spermatogenesis. Spermine confers protection against EMF-associated testicular and reproductive aberrations, at least in part, via antioxidant, anti-inflammatory and anti-apoptotic mechanisms. Excerpt Rats were exposed to the EMF at 900 MHz frequency and 0.02 mW/cm2 power density during 2 h/day over a period of eight consecutive weeks, as previously described (Kesari et al., 2011). The average specific absorption rate was 1.075 W/Kg, as calculated by the Finite-Difference-Time-Domain. Non-exposed rats were placed in the same device with exposure off, used in similar environmental conditions. sciencedirect.com

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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 (male)

Sample sizeNot supplied

ExposureRF · 900 MHz · 1.075 W/kg · 2 h/day for 8 weeks

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Rats exposed to 900 MHz EMF (2 h/day for 8 weeks; power density 0.02 mW/cm2; average SAR 1.075 W/kg) showed decreased sperm count/viability/motility, increased sperm deformities, altered reproductive hormones (including reduced inhibin B and testosterone), reduced steroidogenesis-related markers/enzymes (StAR, c-kit, 3β- and 17β-HSD), increased oxidative/inflammatory/apoptotic markers, and increased testicular DNA damage. Spermine administration (2.5 mg/kg/day i.p. for 8 weeks) prevented or reduced these EMF-associated alterations and was supported by histological findings.

Outcomes measured

Sperm count
Sperm viability
Sperm motility
Sperm deformities
Serum inhibin B
Serum testosterone
Serum activin A
Follicle-stimulating hormone (FSH)
Luteinizing hormone (LH)
Serum estradiol
Testicular StAR expression
Testicular c-kit mRNA expression
Testicular 3β-hydroxysteroid dehydrogenase activity
Testicular 17β-hydroxysteroid dehydrogenase activity
Testicular lipid peroxidation
Catalase activity
Glutathione peroxidase activity
NF-κB p65 expression
iNOS expression
COX-2 expression
Caspase-3 expression
Testicular DNA damage (comet assay parameters)
Testis histology/histomorphometry

Limitations

Sample size not reported in provided abstract/metadata
Exposure source/device type not specified beyond EMF parameters
Animal model; generalizability to humans not established in provided text

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": 900,
    "sar_wkg": 1.075,
    "duration": "2 h/day for 8 weeks"
  },
  "population": "Rats (male)",
  "sample_size": null,
  "outcomes": [
    "Sperm count",
    "Sperm viability",
    "Sperm motility",
    "Sperm deformities",
    "Serum inhibin B",
    "Serum testosterone",
    "Serum activin A",
    "Follicle-stimulating hormone (FSH)",
    "Luteinizing hormone (LH)",
    "Serum estradiol",
    "Testicular StAR expression",
    "Testicular c-kit mRNA expression",
    "Testicular 3β-hydroxysteroid dehydrogenase activity",
    "Testicular 17β-hydroxysteroid dehydrogenase activity",
    "Testicular lipid peroxidation",
    "Catalase activity",
    "Glutathione peroxidase activity",
    "NF-κB p65 expression",
    "iNOS expression",
    "COX-2 expression",
    "Caspase-3 expression",
    "Testicular DNA damage (comet assay parameters)",
    "Testis histology/histomorphometry"
  ],
  "main_findings": "Rats exposed to 900 MHz EMF (2 h/day for 8 weeks; power density 0.02 mW/cm2; average SAR 1.075 W/kg) showed decreased sperm count/viability/motility, increased sperm deformities, altered reproductive hormones (including reduced inhibin B and testosterone), reduced steroidogenesis-related markers/enzymes (StAR, c-kit, 3β- and 17β-HSD), increased oxidative/inflammatory/apoptotic markers, and increased testicular DNA damage. Spermine administration (2.5 mg/kg/day i.p. for 8 weeks) prevented or reduced these EMF-associated alterations and was supported by histological findings.",
  "effect_direction": "harm",
  "limitations": [
    "Sample size not reported in provided abstract/metadata",
    "Exposure source/device type not specified beyond EMF parameters",
    "Animal model; generalizability to humans not established in provided text"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic field",
    "EMF",
    "900 MHz",
    "RF exposure",
    "SAR",
    "rat",
    "male fertility",
    "spermatogenesis",
    "steroidogenesis",
    "testosterone",
    "oxidative stress",
    "inflammation",
    "apoptosis",
    "DNA damage",
    "comet assay",
    "spermine",
    "polyamine"
  ],
  "suggested_hubs": [
    {
      "slug": "rf-male-fertility",
      "weight": 0.9,
      "reason": "Animal study of 900 MHz RF exposure with multiple male reproductive endpoints and protective intervention."
    }
  ]
}

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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.taap.2019.03.009
PubMed: Not supplied

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