Activation of autophagy at cerebral cortex and apoptosis at brainstem are differential responses to 835 MHz RF-EMF exposure
← Research streamAfter 4 weeks of 835 MHz RF-EMF exposure at SAR 4.0 W/kg, increased autophagy-related genes/proteins (including LC3B-II and Beclin1) and accumulation of autophagosomes/autolysosomes were observed in cortical neurons. Apoptosis pathways were up-regulated in th…
Study snapshot
Abstract
Activation of autophagy at cerebral cortex and apoptosis at brainstem are differential responses to 835 MHz RF-EMF exposure Kim JH, Yu DH, Kim HR. Activation of autophagy at cerebral cortex and apoptosis at brainstem are differential responses to 835 MHz RF-EMF exposure. Korean J Physiol Pharmacol. 2017 Mar;21(2):179-188. doi: 10.4196/kjpp.2017.21.2.179. Abstract With the explosive increase in exposure to radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones, public concerns have grown over the last few decades with regard to the potential effects of EMF exposure on the nervous system in the brain. Many researchers have suggested that RF-EMFs can effect diverse neuronal alterations in the brain, thereby affecting neuronal functions as well as behavior. Previously, we showed that long-term exposure to 835 MHz RF-EMF induces autophagy in the mice brain. In this study, we explore whether short-term exposure to RF-EMF leads to the autophagy pathway in the cerebral cortex and brainstem at 835 MHz with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Increased levels of autophagy genes and proteins such as LC3B-II and Beclin1 were demonstrated and the accumulation of autophagosomes and autolysosomes was observed in cortical neurons whereas apoptosis pathways were up- regulated in the brainstem but not in the cortex following 4 weeks of RF exposure. Taken together, the present study indicates that monthly exposure to RF-EMF induces autophagy in the cerebral cortex and suggests that autophagic degradation in cortical neurons against a stress of 835 MHz RF during 4 weeks could correspond to adaptation to the RF stress environment. However, activation of apoptosis rather than autophagy in the brainstem is suggesting the differential responses to the RF-EMF stresses in the brain system. 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
After 4 weeks of 835 MHz RF-EMF exposure at SAR 4.0 W/kg, increased autophagy-related genes/proteins (including LC3B-II and Beclin1) and accumulation of autophagosomes/autolysosomes were observed in cortical neurons. Apoptosis pathways were up-regulated in the brainstem but not in the cortex following RF exposure.
Outcomes measured
- Autophagy markers in cerebral cortex (e.g., LC3B-II, Beclin1; autophagosomes/autolysosomes)
- Apoptosis pathway activation in brainstem
- Regional (cortex vs brainstem) differential response to RF-EMF
Limitations
- Sample size not reported in provided abstract/metadata
- Exposure regimen described as 'short-term' but only 4-week duration details provided; other exposure parameters not specified in provided abstract
- Behavioral/functional outcomes not reported in provided abstract
View raw extracted JSON
{
"study_type": "animal",
"exposure": {
"band": "RF",
"source": "mobile phone",
"frequency_mhz": 835,
"sar_wkg": 4,
"duration": "4 weeks"
},
"population": "Mice",
"sample_size": null,
"outcomes": [
"Autophagy markers in cerebral cortex (e.g., LC3B-II, Beclin1; autophagosomes/autolysosomes)",
"Apoptosis pathway activation in brainstem",
"Regional (cortex vs brainstem) differential response to RF-EMF"
],
"main_findings": "After 4 weeks of 835 MHz RF-EMF exposure at SAR 4.0 W/kg, increased autophagy-related genes/proteins (including LC3B-II and Beclin1) and accumulation of autophagosomes/autolysosomes were observed in cortical neurons. Apoptosis pathways were up-regulated in the brainstem but not in the cortex following RF exposure.",
"effect_direction": "mixed",
"limitations": [
"Sample size not reported in provided abstract/metadata",
"Exposure regimen described as 'short-term' but only 4-week duration details provided; other exposure parameters not specified in provided abstract",
"Behavioral/functional outcomes not reported in provided abstract"
],
"evidence_strength": "low",
"confidence": 0.74,
"peer_reviewed_likely": "yes",
"keywords": [
"RF-EMF",
"835 MHz",
"SAR",
"mouse",
"brain",
"cerebral cortex",
"brainstem",
"autophagy",
"apoptosis",
"LC3B-II",
"Beclin1"
],
"suggested_hubs": [
{
"slug": "mobile-phones",
"weight": 0.85,
"reason": "RF-EMF described as emitted by mobile phones; 835 MHz exposure."
},
{
"slug": "animal-studies",
"weight": 0.8,
"reason": "Mouse brain outcomes following controlled RF exposure."
}
]
}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: 10.4196/kjpp.2017.21.2.179
PubMed: Not supplied
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