Probing Origins of 1,800 MHz RF EMR Induced Damage in Mouse Immortalized Germ Cells and Spermatozoa in vitro

2018 · Mixed · Low evidence

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MixedLow evidencePaper 2003

Study snapshot

Publicationmanual · 2018

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

Probing Origins of 1,800 MHz RF EMR Induced Damage in Mouse Immortalized Germ Cells and Spermatozoa in vitro Houston BJ, Nixon B, King BV, Aitken RJ, De Iuliis GN. Probing the origins of 1,800 MHz radio frequency electromagnetic radiation induced damage in mouse immortalized germ cells and spermatozoa in vitro. Front. Public Health. 2018 Sep 21. doi.org As the use of mobile phone devices is now highly prevalent, many studies have sought to evaluate the effects of the radiofrequency-electromagnetic radiation (RF-EMR) on both human health and biology. While several such studies have shown RF-EMR is capable of inducing cellular stress, the physicobiological origin of this stress remains largely unresolved. To explore the effect of RF-EMR on the male reproductive system, we exposed cultured mouse spermatogonial GC1 and spermatocyte GC2 cell lines, as well as cauda epididymal spermatozoa to a waveguide generating continuous wave RF-EMR (1.8 GHz, 0.15 and 1.5 W/kg). This study demonstrated that a 4 h exposure is capable of inducing the generation of mitochondrial reactive oxygen species (ROS) in populations of GC1 (7 vs. 18%; p < 0.001) and GC2 cells (11.5 vs. 16 %; p < 0.01), identifying Complex III of the electron transport chain (ETC) as the potential source of electrons producing ROS. Assessing the generation of ROS in the presence of an antioxidant, penicillamine, as well as measuring lipid peroxidation via 4- hydroxynonenal levels, indicated that the elevated incidence of ROS generation observed under our exposure conditions did not necessarily induce an overt cellular oxidative stress response. However, exposure to RF-EMR at 0.15 W/kg for 3 h did induce significant DNA fragmentation in spermatozoa (that was no longer significant after 4 h), assessed by the alkaline comet assay (p < 0.05). Furthermore, this fragmentation was accompanied by an induction of oxidative DNA damage in the form of 8-hydroxy-2′-deoxyguanosine, which was significant (p < 0.05) after spermatozoa were exposed to RF-EMR for 4 h. At this exposure time point, a decline in sperm motility (p < 0.05) was also observed. This study contributes new evidence toward elucidating a mechanism to account for the effects of RF-EMR on biological systems, proposing Complex III of the mitochondrial ETC as the key target of this radiation. Open access paper: frontiersin.org

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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 typein_vitro

Effect directionmixed

PopulationMouse immortalized germ cell lines (GC1 spermatogonia; GC2 spermatocytes) and mouse cauda epididymal spermatozoa (in vitro)

Sample sizeNot supplied

ExposureRF · 1800 MHz · 3–4 h

Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

Continuous-wave 1.8 GHz RF-EMR exposure (0.15 and 1.5 W/kg) for 4 h increased mitochondrial ROS generation in GC1 and GC2 cells, with results suggesting Complex III of the mitochondrial ETC as a potential source. In spermatozoa, RF-EMR at 0.15 W/kg induced significant DNA fragmentation after 3 h (not significant after 4 h), while oxidative DNA damage (8-hydroxy-2′-deoxyguanosine) was significant after 4 h and sperm motility declined at 4 h.

Outcomes measured

Mitochondrial reactive oxygen species (ROS) generation
Electron transport chain (ETC) Complex III as potential ROS source
Lipid peroxidation (4-hydroxynonenal)
DNA fragmentation in spermatozoa (alkaline comet assay)
Oxidative DNA damage (8-hydroxy-2′-deoxyguanosine)
Sperm motility

Limitations

Sample size not reported in provided abstract/metadata
In vitro model (cell lines and isolated spermatozoa) may not generalize to in vivo exposures
Exposure conditions limited to continuous-wave 1.8 GHz and specific SARs (0.15, 1.5 W/kg) and short durations (3–4 h)

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": "RF",
    "source": "mobile phone",
    "frequency_mhz": 1800,
    "sar_wkg": null,
    "duration": "3–4 h"
  },
  "population": "Mouse immortalized germ cell lines (GC1 spermatogonia; GC2 spermatocytes) and mouse cauda epididymal spermatozoa (in vitro)",
  "sample_size": null,
  "outcomes": [
    "Mitochondrial reactive oxygen species (ROS) generation",
    "Electron transport chain (ETC) Complex III as potential ROS source",
    "Lipid peroxidation (4-hydroxynonenal)",
    "DNA fragmentation in spermatozoa (alkaline comet assay)",
    "Oxidative DNA damage (8-hydroxy-2′-deoxyguanosine)",
    "Sperm motility"
  ],
  "main_findings": "Continuous-wave 1.8 GHz RF-EMR exposure (0.15 and 1.5 W/kg) for 4 h increased mitochondrial ROS generation in GC1 and GC2 cells, with results suggesting Complex III of the mitochondrial ETC as a potential source. In spermatozoa, RF-EMR at 0.15 W/kg induced significant DNA fragmentation after 3 h (not significant after 4 h), while oxidative DNA damage (8-hydroxy-2′-deoxyguanosine) was significant after 4 h and sperm motility declined at 4 h.",
  "effect_direction": "mixed",
  "limitations": [
    "Sample size not reported in provided abstract/metadata",
    "In vitro model (cell lines and isolated spermatozoa) may not generalize to in vivo exposures",
    "Exposure conditions limited to continuous-wave 1.8 GHz and specific SARs (0.15, 1.5 W/kg) and short durations (3–4 h)"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "RF-EMR",
    "1.8 GHz",
    "1800 MHz",
    "SAR",
    "GC1",
    "GC2",
    "spermatozoa",
    "mitochondrial ROS",
    "Complex III",
    "electron transport chain",
    "DNA fragmentation",
    "8-hydroxy-2′-deoxyguanosine",
    "sperm motility",
    "oxidative stress"
  ],
  "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: 10.3389/fpubh.2018.00270
PubMed: Not supplied

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