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p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic field exposure

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Zhang Y, She F, Li L, Chen C, Xu S, Luo X, Li M, He M, Yu Z. · 2013

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The results suggest that abnormal p25/CDK5 activity is partially involved in injury to primary cultured cortical neurons from newborn Sprague-Dawley rats exposed to RF-EMF.

Plain English Summary

Summary written for general audiences

Researchers exposed primary cultured cortical neurons from newborn Sprague-Dawley rats to pulsed 2.45 GHz radiofrequency electromagnetic fields for 10 minutes. Exposure significantly decreased cellular viability and increased apoptotic nuclei, CDK5 activity, the p25 to p35 ratio, and tau phosphorylation at Ser404. CDK5 expression did not change significantly after exposure. A CDK5 inhibitor blocked the exposure-induced decrease in cellular viability and tau hyperphosphorylation but did not significantly block apoptosis.

Why This Matters

Cellular viability was measured with an MTT assay, apoptosis with Hoechst 33342 and TUNEL co-staining, protein levels by Western blot, and CDK5 activity by a histone-H1 kinase assay. The authors suggest that abnormal p25/CDK5 activity is partially involved in injury to primary cultured cortical neurons from newborn Sprague-Dawley rats exposed to RF-EMF.

Exposure Information

A logarithmic frequency spectrum from 10 Hz to 100 GHz showing where this study's 2.45 GHz exposure sits relative to common EMF sources.Where This Frequency Sits on the EMF SpectrumELFVLFLF / MFHF / VHFUHFSHFmm10 Hz100 GHzThis study: 2.45 GHzPower lines50/60 Hz5G mm28 GHzLogarithmic scale

Specific exposure levels were not quantified in this study. The study examined exposure from: 2.45 GHz RF-EMF Duration: 10 min

Study Details

The aim of the present work was to investigate whether the cyclin-dependent kinase 5 (CDK5) pathway is involved in neuronal injury induced by RF-EMF exposure.

Newborn Sprague-Dawley rats’ primary cultured cortical neurons were exposed to pulsed 2.45 GHz RF-EM...

The cellular viability of neurons was significantly decreased (p < 0.01, Partial Eta Squared [ηp2]: ...

These results suggest that abnormal activity of p25/CDK5 is partially involved in primary cultured cortical neuron injury induced by RF-EMF exposure.

Cite This Study
Zhang Y, She F, Li L, Chen C, Xu S, Luo X, Li M, He M, Yu Z. (2013). p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic field exposure Int J Radiat Biol 2013; 89 (11): 976-984.
Show BibTeX
@article{y_2013_p25cdk5_is_partially_involved_1550,
  author = {Zhang Y and She F and Li L and Chen C and Xu S and Luo X and Li M and He M and Yu Z.},
  title = {p25/CDK5 is partially involved in neuronal injury induced by radiofrequency electromagnetic field exposure},
  year = {2013},
  doi = {10.3109/09553002.2013.817699},
  url = {https://www.tandfonline.com/doi/abs/10.3109/09553002.2013.817699},
}
DOI: 10.3109/09553002.2013.817699

Cited By (9 papers)

Quick Questions About This Study

Primary cultured cortical neurons from newborn Sprague-Dawley rats were exposed to pulsed 2.45 GHz radiofrequency electromagnetic fields for 10 minutes.
Exposure significantly decreased cellular viability and increased apoptotic nuclei, CDK5 activity, the p25 to p35 ratio, and tau phosphorylation at Ser404.
No significant change was detected in CDK5 expression after exposure.
A CDK5 inhibitor blocked the exposure-induced decrease in cellular viability and tau hyperphosphorylation but did not significantly block apoptosis.
The results suggest that abnormal p25/CDK5 activity is partially involved in injury to primary cultured cortical neurons from newborn Sprague-Dawley rats exposed to RF-EMF.