Del Vecchio, G.; Giuliani, A.; Fernandez, M.; Mesirca, P.; Bersani, F.; Pinto, R.; Ardoino, L.; Lovisolo, G. A.; Giardino, L., and Calza, L. Effect of radiofrequency electromagnetic field exposure on in vitro models of neurodegenerative disease. Bioelectromagnetics. 2009 May 28.

Effects of exposure to pulsed global system for mobile telecommunication microwaves (GSM) to the central nervous system have been explored in studies ranging from epidemiology to molecular studies. However, the possible effect of EMF exposure as a co-stressor for chemical challenges including neurodegeneration has not been sufficiently explored.

The objective of this study was to investigate whether continuous exposure to 900 MHz GSM modulated EMF affects viability, proliferation and vulnerability of neural cells to different toxic stimuli.

Two cellular systems were used in this study: rat primary cortical neurons and SN56 line. Cells were exposed to GSM modulated 900 MHz signal at SAR of 1 W/kg and maximum duration of 144 hours. The cells were treated with 25-35AA beta-amyloid (as an in vitro model for Alzheimer disease), glutamate (as a model for excitotoxicity), and H2O2 (as a model for oxidative stress). The following effects were studied in these experiments: for SN56 line (cells that retain the ability to proliferate) - proliferation curve, nuclear morphology, the effects of co-exposure to RF and H2O2 and co-exposure to RF and beta-amyloid; for primary cortical neurons (non-proliferating cells) - cell viability, nuclear morphology, the effects of co-exposure to RF and H2O2 and co-exposure to RF and glutamate.

Exposure to RF did not alter viability/proliferation rate of the cells. The only situation in which the EMF exposure acted as a co-stressor was cell death induced by H2O2 in the SN56 cell line. No similar effect was observed in primary cortical neurons.

Interpretation and conclusion
The results of this study suggest that exposure to 900 MHz GSM modulated EMF slightly increases vulnerability of SN56 cells to oxidative stress and has no effect on the glutamate and beta-amyloid dependent cell death.

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