Involvement of mitochondrial activity in mediating ELF-EMF stimulatory effect on human sperm motility.
← Research streamExposure to 50 Hz, 5 mT ELF-EMF increased mitochondrial membrane potential, ATP, ADP, NAD(+) levels, and sperm motility parameters. Inhibition experiments indicated mitochondrial oxidative phosphorylation mediates the stimulatory effect rather than glycolysis.
Study snapshot
Abstract
It has recently been reported that the exposure of human spermatozoa to an extremely low frequency (ELF) electromagnetic field (EMF) with a square waveform of 5 mT amplitude and frequency of 50 Hz improves sperm motility. The functional relationship between the energy metabolism and the enhancement of human sperm motility induced by ELF-EMF was investigated. Sperm exposure to ELF-EMF resulted in a progressive and significant increase of mitochondrial membrane potential and levels of ATP, ADP and NAD(+) that was associated with a progressive and significant increase in the sperm kinematic parameters. No significant effects were detected on other parameters such as ATP/ADP ratio and energy charge. When carbamoyl cyanide m-chlorophenylhydrazone (CICCP) was applied to inhibit the oxidative phosphorylation in the mitochondria, the values of energy parameters and motility in the sperm incubated in the presence of glucose and exposed to ELF-EMF did not change, thus indicating that the glycolysis was not involved in mediating ELF-EMF stimulatory effect on motility. By contrast, when pyruvate and lactate were provided instead of glucose, the energy status and motility increased significantly in ELF-EMF-treated sperm. Under these culture conditions, the inhibition of glycolitic metabolism by 2-deoxy-D-glucose (DOG) again resulted in increased values of energy and kinematic parameters, indicating that gluconeogenesis was not involved in producing glucose for use in glycolysis. We concluded that the key role in mediating the stimulatory effects exerted by ELF-EMF on human sperm motility is played by mitochondrial oxidative phosphorylation rather than glycolysis.
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
Exposure to 50 Hz, 5 mT ELF-EMF increased mitochondrial membrane potential, ATP, ADP, NAD(+) levels, and sperm motility parameters. Inhibition experiments indicated mitochondrial oxidative phosphorylation mediates the stimulatory effect rather than glycolysis.
Outcomes measured
- sperm motility
- mitochondrial membrane potential
- ATP levels
- ADP levels
- NAD(+) levels
- sperm kinematic parameters
- ATP/ADP ratio
- energy charge
Limitations
- No sample size reported
- In vitro study limits generalizability to in vivo conditions
- No long-term exposure effects assessed
View raw extracted JSON
{
"study_type": "in_vitro",
"exposure": {
"band": "ELF",
"source": null,
"frequency_mhz": 0.05,
"sar_wkg": null,
"duration": null
},
"population": "human spermatozoa",
"sample_size": null,
"outcomes": [
"sperm motility",
"mitochondrial membrane potential",
"ATP levels",
"ADP levels",
"NAD(+) levels",
"sperm kinematic parameters",
"ATP/ADP ratio",
"energy charge"
],
"main_findings": "Exposure to 50 Hz, 5 mT ELF-EMF increased mitochondrial membrane potential, ATP, ADP, NAD(+) levels, and sperm motility parameters. Inhibition experiments indicated mitochondrial oxidative phosphorylation mediates the stimulatory effect rather than glycolysis.",
"effect_direction": "benefit",
"limitations": [
"No sample size reported",
"In vitro study limits generalizability to in vivo conditions",
"No long-term exposure effects assessed"
],
"evidence_strength": "moderate",
"confidence": 0.7,
"peer_reviewed_likely": "yes",
"keywords": [
"ELF-EMF",
"human sperm motility",
"mitochondrial activity",
"oxidative phosphorylation",
"energy metabolism"
],
"suggested_hubs": []
}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/bem.20602
PubMed: 20690107
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