Role of Mitochondria in the Oxidative Stress Induced by EMF: Focus on Reproductive Systems
← Research streamThis review summarizes literature suggesting EMF exposure can alter redox-related processes in reproductive systems, with mitochondria proposed as a key source of ROS. The authors report contradictory findings across studies due to non-uniform experimental de…
Study snapshot
Abstract
Role of Mitochondria in the Oxidative Stress Induced by EMF: Focus on Reproductive Systems Santini SJ, Cordone V, Falone S, Mijit M, Tatone C, Amicarelli F, Di Emidio G. Role of mitochondria in the oxidative stress induced by electromagnetic fields: Focus on reproductive systems. Oxid Med Cell Longev. 2018 Nov 8;2018:5076271. doi: 10.1155/2018/5076271. Abstract Modern technologies relying on wireless communication systems have brought increasing levels of electromagnetic field (EMF) exposure. This increased research interest in the effects of these radiations on human health. There is compelling evidence that EMFs affect cellphysiology by altering redox-related processes. Considering the importance of redox milieu in the biological competence of oocyte and sperm, we reviewed the existing literature regarding the effects of EMFs on reproductive systems. Given the role of mitochondria as the main source of reactive oxygen species (ROS), we focused on the hypothesis of a mitochondrial basis of EMF- induced reproductive toxicity. MEDLINE, Web of Science, and Scopus database were examined for peer- reviewed original articles by searching for the following keywords: "extremely low frequency electromagnetic fields (ELF-EMFs)," "radiofrequency (RF)," "microwaves," "Wi-Fi," "mobile phone," "oxidative stress," "mitochondria," "fertility," "sperm," "testis," "oocyte," "ovarian follicle," and "embryo." These keywords were combined with other search phrases relevant to the topic. Although we reported contradictory data due to lack of uniformity in the experimental designs, a growing body of evidence suggests that EMF exposure during spermatogenesis induces increased ROS production associated with decreased ROS scavenging activity. Numerous studies revealed the detrimental effects of EMFs from mobile phones, laptops, and other electric devices on sperm quality and provide evidence for extensive electron leakage from the mitochondrial electron transport chain as the main cause of EMF damage. In female reproductive systems, the contribution of oxidative stress to EMF-induced damages and the evidence of mitochondrial origin of ROS overproduction are reported, as well. In conclusion, mitochondria seem to play an important role as source of ROS in both male and female reproductive systems under EMF exposure. Future and more standardized studies are required for a better understanding of molecular mechanisms underlying EMF potential challenge to our reproductive system in order to improve preventive strategies. Open access paper: ncbi.nlm.nih.gov
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.
Main findings
This review summarizes literature suggesting EMF exposure can alter redox-related processes in reproductive systems, with mitochondria proposed as a key source of ROS. The authors report contradictory findings across studies due to non-uniform experimental designs, but describe a growing body of evidence linking EMF exposure during spermatogenesis to increased ROS production and decreased ROS scavenging activity, and report detrimental effects on sperm quality in multiple studies.
Outcomes measured
- oxidative stress
- mitochondria/mitochondrial electron transport chain effects
- reactive oxygen species (ROS) production
- ROS scavenging activity
- sperm quality
- fertility/reproductive toxicity
Limitations
- Contradictory data reported across studies
- Lack of uniformity/standardization in experimental designs
- Calls for future, more standardized studies to clarify mechanisms
View raw extracted JSON
{
"study_type": "review",
"exposure": {
"band": null,
"source": "wireless communication systems; mobile phone; Wi‑Fi; laptops; other electric devices",
"frequency_mhz": null,
"sar_wkg": null,
"duration": null
},
"population": "Reproductive systems (male and female; sperm, testis, oocyte, ovarian follicle, embryo)",
"sample_size": null,
"outcomes": [
"oxidative stress",
"mitochondria/mitochondrial electron transport chain effects",
"reactive oxygen species (ROS) production",
"ROS scavenging activity",
"sperm quality",
"fertility/reproductive toxicity"
],
"main_findings": "This review summarizes literature suggesting EMF exposure can alter redox-related processes in reproductive systems, with mitochondria proposed as a key source of ROS. The authors report contradictory findings across studies due to non-uniform experimental designs, but describe a growing body of evidence linking EMF exposure during spermatogenesis to increased ROS production and decreased ROS scavenging activity, and report detrimental effects on sperm quality in multiple studies.",
"effect_direction": "mixed",
"limitations": [
"Contradictory data reported across studies",
"Lack of uniformity/standardization in experimental designs",
"Calls for future, more standardized studies to clarify mechanisms"
],
"evidence_strength": "low",
"confidence": 0.74,
"peer_reviewed_likely": "yes",
"keywords": [
"electromagnetic fields",
"ELF-EMF",
"radiofrequency",
"microwaves",
"Wi-Fi",
"mobile phone",
"oxidative stress",
"mitochondria",
"reactive oxygen species",
"fertility",
"sperm",
"testis",
"oocyte",
"ovarian follicle",
"embryo",
"reproductive toxicity"
],
"suggested_hubs": [
{
"slug": "school-wi-fi",
"weight": 0.22,
"reason": "Wi‑Fi is explicitly included among exposures searched/discussed."
}
]
}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: 10.1155/2018/5076271
PubMed: Not supplied
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