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Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: Molecular mechanism for cancer- and blood-brain barrier-related effects.

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Leszczynski D, Joenväärä S, Reivinen J, Kuokka R · 2002

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One-hour non-thermal exposure to 900 MHz GSM radiation transiently increased hsp27 phosphorylation in human endothelial cells, an effect blocked by a p38MAPK inhibitor.

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Researchers exposed human endothelial EA.hy926 cells to 900 MHz GSM mobile phone radiation for 1-hour and observed changes in phosphorylation of many proteins. The exposure transiently increased phosphorylation of hsp27 and altered expression levels of hsp27 and p38MAPK, and this phosphorylation increase was prevented by a p38MAPK inhibitor. The culture temperature remained at 37 +/- 0.3 degrees C throughout the exposure, confirming non-thermal effects. The authors hypothesized that mobile phone radiation-induced activation of hsp27 may facilitate brain cancer by inhibiting the cytochrome c/caspase-3 apoptotic pathway and increase blood-brain barrier permeability by stabilizing endothelial cell stress fibers.

Study Details

We have examined whether non-thermal exposures of cultures of the human endothelial cell line EA.hy926 to 900 MHz GSM mobile phone microwave radiation could activate stress response.

Results obtained demonstrate that 1-hour non-thermal exposure of EA.hy926 cells changes the phosphor...

Based on the known functions of hsp27, we put forward the hypothesis that mobile phone radiation-induced activation of hsp27 may (i) facilitate the development of brain cancer by inhibiting the cytochrome c/caspase-3 apoptotic pathway and (ii) cause an increase in blood-brain barrier permeability through stabilization of endothelial cell stress fibers. We postulate that these events, when occurring repeatedly over a long period of time, might become a health hazard because of the possible accumulation of brain tissue damage. Furthermore, our hypothesis suggests that other brain damaging factors may co-participate in mobile phone radiation-induced effects.

Cite This Study
Leszczynski D, Joenväärä S, Reivinen J, Kuokka R (2002). Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: Molecular mechanism for cancer- and blood-brain barrier-related effects. Differentiation 70:120–129, 2002.
Show BibTeX
@article{d_2002_nonthermal_activation_of_the_2352,
  author = {Leszczynski D and Joenväärä S and Reivinen J and Kuokka R},
  title = {Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: Molecular mechanism for cancer- and blood-brain barrier-related effects.},
  year = {2002},
  
  url = {https://pubmed.ncbi.nlm.nih.gov/12076339/},
}
PubMed: 12076339

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Quick Questions About This Study

Human endothelial EA.hy926 cells were used.
The cells were exposed to 900 MHz GSM radiation for 1-hour.
No, the temperature remained at 37 +/- 0.3 degrees C throughout the exposure, confirming non-thermal effects.
Exposure transiently increased phosphorylation of hsp27 and altered expression levels of hsp27 and p38MAPK, and the phosphorylation increase was blocked by a p38MAPK inhibitor.
They hypothesized that mobile phone radiation-induced activation of hsp27 may facilitate brain cancer by inhibiting the cytochrome c/caspase-3 apoptotic pathway and increase blood-brain barrier permeability by stabilizing endothelial cell stress fibers. They also postulated that repeated long-term exposure might become a health hazard due to possible accumulation of brain tissue damage.