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Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats.

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Ertilav K, Uslusoy F, Ataizi S, Nazıroğlu M. · 2018

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Rats exposed to 900 and 1800 MHz EMR for 60 minutes per day, five days per week, for one year showed increased TRPV1 currents, calcium influx, ROS, mitochondrial depolarization, apoptosis, and caspase activity, with greater effects at 1800 MHz.

Plain English Summary

Summary written for general audiences

Twenty-four adult rats were divided into control, 900 MHz, and 1800 MHz exposure groups. Each experimental group was exposed to electromagnetic radiation for 60 minutes per day, five days per week, for one year. Both frequencies increased TRPV1 currents, calcium influx, reactive oxygen species, mitochondrial membrane depolarization, apoptosis, and caspase 3 and 9 activities in the hippocampus and dorsal root ganglion. The 1800 MHz exposure produced greater increases in these measures than the 900 MHz exposure.

Why This Matters

The study investigated the contribution of TRPV1 to mitochondrial oxidative stress and apoptosis in the hippocampus and dorsal root ganglion after long-term exposure to 900 and 1800 MHz in rats. The researchers concluded that mitochondrial oxidative stress, programmed cell death, and calcium entry through TRPV1 activation in the hippocampus and dorsal root ganglion of rats were increased after exposure to 900 and 1800 MHz cell frequencies. The results suggest that exposure to 900 and 1800 MHz EMR may induce a dose-associated, TRPV1-mediated stress response.

Exposure Information

A logarithmic frequency spectrum from 10 Hz to 100 GHz showing where this study's 1.80 GHz exposure sits relative to common EMF sources.Where This Frequency Sits on the EMF SpectrumELFVLFLF / MFHF / VHFUHFSHFmm10 Hz100 GHzThis study: 1.80 GHzPower lines50/60 Hz5G mm28 GHzLogarithmic scale

Specific exposure levels were not quantified in this study. The study examined exposure from: 900 and 1800 MHz Duration: 60 min/ 5 days of the week during the one year

Study Details

We investigated the contribution TRPV1 to mitochondrial oxidative stress and apoptosis in HIPPON and DRGN following long term exposure to 900 and 1800 MHz in a rat model

Twenty-four adult rats were equally divided into the following groups: (1) control, (2) 900 MHz, and...

The 900 and 1800 MHz EMR exposure induced increases in TRPV1 currents, intracellular free calcium in...

In conclusion, mitochondrial oxidative stress, programmed cell death and Ca2+ entry pathway through TRPV1 activation in the HIPPON and DRGN of rats were increased in the rat model following exposure to 900 and 1800 MHz cell frequencies. Our results suggest that exposure to 900 and 1800 MHz EMR may induce a dose-associated, TRPV1-mediated stress response.

Cite This Study
Ertilav K, Uslusoy F, Ataizi S, Nazıroğlu M. (2018). Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats. Metab Brain Dis. 33(3):753-763, 2018. Jan 13.
Show BibTeX
@article{k_2018_long_term_exposure_to_1632,
  author = {Ertilav K and Uslusoy F and Ataizi S and Nazıroğlu M.},
  title = {Long term exposure to cell phone frequencies (900 and 1800 MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats.},
  year = {2018},
  doi = {10.1007/s11011-017-0180-4},
  url = {https://link.springer.com/article/10.1007/s11011-017-0180-4},
}
DOI: 10.1007/s11011-017-0180-4

Quick Questions About This Study

Rats were divided into control, 900 MHz, and 1800 MHz exposure groups. Each exposure group received 60 minutes of EMR per day, five days per week, for one year.
The study measured TRPV1 currents, intracellular calcium influx, reactive oxygen species production, mitochondrial membrane depolarization, apoptosis, and caspase 3 and 9 activities in the hippocampus and dorsal root ganglion.
The 1800 MHz exposure produced greater increases in all measured deleterious processes compared to the 900 MHz exposure.
The results indicate that TRPV1 channel activation mediated calcium entry, mitochondrial oxidative stress, and programmed cell death in response to the electromagnetic exposure.
The researchers concluded that mitochondrial oxidative stress, programmed cell death, and calcium entry through TRPV1 activation in the hippocampus and dorsal root ganglion of rats were increased after exposure to 900 and 1800 MHz cell frequencies.