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Exposure to 835 MHz radiofrequency electromagnetic field induces autophagy in hippocampus but not in brain stem of mice.

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Kim JH, Yu DH, Kim HJ, Huh YH, Cho SW, Lee JK, Kim HG, Kim HR. · 2017

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Exposure to 835 MHz RF-EMF at 4.0 W/kg for 12 weeks induced autophagy in the hippocampus of mice, but not in the brain stem.

Plain English Summary

Summary written for general audiences

Researchers exposed C57BL/6 mice to 835 MHz RF-EMF at an SAR of 4.0 W/kg for 12 weeks, then analyzed the hippocampus and brain stem. Several autophagic genes were significantly upregulated only in the hippocampus and not in the brain stem. Transmission electron microscopy revealed an increase in the number of autophagosomes and autolysosomes in the hippocampal neurons of exposed mice.

Why This Matters

The researchers explored whether autophagy is triggered in the hippocampus or brain stem after RF-EMF exposure. Gene activity was measured using quantitative real-time polymerase chain reaction, and key regulatory proteins LC3B-II and p62 were also assessed. Both the gene expression changes and the protein level changes were significant only in the hippocampus, not in the brain stem. The researchers suggested that autophagic degradation may be one possible mechanism by which specific brain regions adapt to an RF-EMF exposure environment.

Exposure Details

SAR
4 W/kg
Source/Device
835 MHz
Exposure Duration
12 weeks

Exposure Context

This study used 4 W/kg for SAR (device absorption):

Building Biology guidelines are practitioner-based limits from real-world assessments. BioInitiative Report recommendations are based on peer-reviewed science. Check Your Exposure to compare your own measurements.

Where This Falls on the Concern Scale

Study Exposure Level in ContextStudy Exposure Level in ContextThis study: 4 W/kgExtreme Concern - 0.1 W/kgFCC Limit - 1.6 W/kgEffects observed in the Extreme Concern range (Building Biology)This level is 3 times the FCC limit
A logarithmic frequency spectrum from 10 Hz to 100 GHz showing where this study's 835 MHz exposure sits relative to common EMF sources.Where This Frequency Sits on the EMF SpectrumELFVLFLF / MFHF / VHFUHFSHFmm10 Hz100 GHzThis study: 835 MHzPower lines50/60 Hz5G mm28 GHzLogarithmic scale

Study Details

In the present study, we explored whether autophagy is triggered in the hippocampus or brain stem after RF-EMF exposure.

C57BL/6 mice were exposed to 835 MHz RF-EMF with specific absorption rates (SAR) of 4.0 W/kg for 12 ...

Quantitative real-time polymerase chain reaction (qRT-PCR) analysis demonstrated that several autoph...

These results could suggest that among the various adaptation processes to the RF-EMF exposure environment, autophagic degradation is one possible mechanism in specific brain regions.

Cite This Study
Kim JH, Yu DH, Kim HJ, Huh YH, Cho SW, Lee JK, Kim HG, Kim HR. (2017). Exposure to 835 MHz radiofrequency electromagnetic field induces autophagy in hippocampus but not in brain stem of mice. Toxicol Ind Health. 2017 Jan 1:748233717740066. doi: 10.1177/0748233717740066.
Show BibTeX
@article{jh_2017_exposure_to_835_mhz_1103,
  author = {Kim JH and Yu DH and Kim HJ and Huh YH and Cho SW and Lee JK and Kim HG and Kim HR.},
  title = {Exposure to 835 MHz radiofrequency electromagnetic field induces autophagy in hippocampus but not in brain stem of mice.},
  year = {2017},
  
  url = {https://pubmed.ncbi.nlm.nih.gov/29166827/},
}
PubMed: 29166827

Cited By (26 papers)

Quick Questions About This Study

C57BL/6 mice were exposed to 835 MHz RF-EMF at an SAR of 4.0 W/kg for 12 weeks.
Autophagy was not induced in the brain stem; the autophagic gene and protein changes were found only in the hippocampus.
Transmission electron microscopy revealed an increase in the number of autophagosomes and autolysosomes in the hippocampal neurons of RF-EMF-exposed mice.
The researchers suggested that autophagic degradation is one possible mechanism among various adaptation processes to the RF-EMF exposure environment, occurring in specific brain regions.
The study measured expression levels of LC3B-II protein and p62, described as crucial autophagic regulatory proteins.