The effect of exposure to radiofrequency LTE signal and coexposure to mitomycin-C in Chinese hamster lung fibroblast V79 cells
← Research streamRF exposure alone (1950 MHz LTE) at SAR 0.3 and 1.25 W/kg showed no differences versus sham for micronuclei, ROS, or cell cycle progression across tested conditions. With RF pre-exposure followed by MMC, 3 h pre-exposure did not modify MMC-induced micronuclei…
Study snapshot
Abstract
The effect of exposure to radiofrequency LTE signal and coexposure to mitomycin-C in Chinese hamster lung fibroblast V79 cells Sannino A, Romeo S, Scarfì MR, Pinchera D, Schettino F, Alonzo M, Allocca M, Zeni O. Sannino A, Romeo S, Scarfì MR, Pinchera D, Schettino F, Alonzo M, Allocca M, Zeni O. The effect of exposure to radiofrequency LTE signal and coexposure to mitomycin-C in Chinese hamster lung fibroblast V79 cells. Bioelectromagnetics. 2023 Jul 26. doi: 10.1002/bem.22478 . Bioelectromagnetics. 2023 Jul 26. doi: 10.1002/bem.22478 Abstract This study aims to investigate the cellular effects of radiofrequency exposure, 1950 MHz, long-term evolution (LTE) signal, administered alone and in combination with mitomycin-C (MMC), a well-known cytotoxic agent. Chinese hamster lung fibroblast (V79) cells were exposed/sham exposed in a waveguide-based system under strictly controlled conditions of both electromagnetic and environmental parameters, at specific absorption rate (SAR) of 0.3 and 1.25 W/kg. Chromosomal damage (micronuclei formation), oxidative stress (reactive oxygen species [ROS] formation), and cell cycle progression were analyzed after exposure and coexposure. No differences between exposed samples and sham-controls were detected following radiofrequency exposure alone, for all the experimental conditions tested and biological endpoints investigated. When radiofrequency exposure was followed by MMC treatment, 3 h pre-exposure did not modify MMC-induced micronuclei. Pre- exposure of 20 h at 0.3 W/kg did not modify the number of micronuclei induced by MMC, while 1.25 W/kg resulted in a significant reduction of MMC-induced damage. Absence of effects was also detected when CW was used, at both SAR levels. MMC-induced ROS formation resulted significantly decreased at both SAR levels investigated, while cell proliferation and cell cycle progression were not affected by coexposures. The results here reported provide no evidence of direct effects of 1950 MHz, LTE signal. Moreover, they further support our previous findings on the capability of radiofrequency pre-exposure to induce protection from a subsequent toxic treatment, and the key role of the modulated signals and the experimental conditions adopted in eliciting the effect. pubmed.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
RF exposure alone (1950 MHz LTE) at SAR 0.3 and 1.25 W/kg showed no differences versus sham for micronuclei, ROS, or cell cycle progression across tested conditions. With RF pre-exposure followed by MMC, 3 h pre-exposure did not modify MMC-induced micronuclei; 20 h pre-exposure at 0.3 W/kg did not modify MMC-induced micronuclei, while 20 h at 1.25 W/kg significantly reduced MMC-induced micronuclei. MMC-induced ROS formation was significantly decreased at both SAR levels, and cell proliferation/cell cycle progression were not affected by coexposures; no effects were detected when CW was used at both SAR levels.
Outcomes measured
- Chromosomal damage (micronuclei formation)
- Oxidative stress (reactive oxygen species [ROS] formation)
- Cell cycle progression
- Cell proliferation
Limitations
- In vitro cell model (V79 cells); generalizability to humans not addressed in abstract
- Sample size not reported in abstract
- Exposure durations and conditions limited to those tested (3 h and 20 h; SAR 0.3 and 1.25 W/kg; LTE and CW)
View raw extracted JSON
{
"study_type": "in_vitro",
"exposure": {
"band": "RF",
"source": "LTE signal (radiofrequency exposure in waveguide-based system)",
"frequency_mhz": 1950,
"sar_wkg": null,
"duration": "3 h and 20 h pre-exposure; exposure alone and pre-exposure followed by mitomycin-C (MMC)"
},
"population": "Chinese hamster lung fibroblast (V79) cells",
"sample_size": null,
"outcomes": [
"Chromosomal damage (micronuclei formation)",
"Oxidative stress (reactive oxygen species [ROS] formation)",
"Cell cycle progression",
"Cell proliferation"
],
"main_findings": "RF exposure alone (1950 MHz LTE) at SAR 0.3 and 1.25 W/kg showed no differences versus sham for micronuclei, ROS, or cell cycle progression across tested conditions. With RF pre-exposure followed by MMC, 3 h pre-exposure did not modify MMC-induced micronuclei; 20 h pre-exposure at 0.3 W/kg did not modify MMC-induced micronuclei, while 20 h at 1.25 W/kg significantly reduced MMC-induced micronuclei. MMC-induced ROS formation was significantly decreased at both SAR levels, and cell proliferation/cell cycle progression were not affected by coexposures; no effects were detected when CW was used at both SAR levels.",
"effect_direction": "mixed",
"limitations": [
"In vitro cell model (V79 cells); generalizability to humans not addressed in abstract",
"Sample size not reported in abstract",
"Exposure durations and conditions limited to those tested (3 h and 20 h; SAR 0.3 and 1.25 W/kg; LTE and CW)"
],
"evidence_strength": "low",
"confidence": 0.78,
"peer_reviewed_likely": "yes",
"keywords": [
"1950 MHz",
"LTE",
"radiofrequency",
"SAR",
"V79 cells",
"micronuclei",
"ROS",
"oxidative stress",
"mitomycin-C",
"coexposure",
"adaptive response",
"waveguide-based exposure system"
],
"suggested_hubs": [
{
"slug": "who-icnirp",
"weight": 0.2,
"reason": "RF exposure study reporting SAR levels and biological endpoints relevant to RF health evidence base."
}
]
}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.22478
PubMed: 37493434
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