Giovanna Del Vecchio1, Alessandro Giuliani1, Mercedes Fernandez1, Pietro Mesirca2, Ferdinando Bersani2, Rosanna Pinto3, Lucia Ardoino3, Giorgio A. Lovisolo3, Luciana Giardino1,4 and Laura Calza1,4
1Department of Veterinary Morphophysiology and Animal Production (DIMORFIPA), Bologna University, Bologna, Italy
2Department of Physics, Bologna University, Bologna, Italy
3Toxicology and Biomedical Sciences Unit, C. R. Casaccia ENEA, Rome, Italy
4INBB, Bologna University, Bologna, Italy
Summary of research published in Biolelectromagnetics, Vol. 30, No. 7, pp 564-572.
The incidence of neurodegenerative diseases is progressively increasing, partially due to the increase in life expectancy. However, pathogenesis of many neurodegenerative diseases including Alzheimer disease (AD) is still obscure. Among potential environmental risk factors for AD, exposures to electromagnetic fields (EMF) have received much attention, particularly extremely low frequency electromagnetic fields (ELF-EMF). The main approach in these studies has been the systematic review and meta-analysis of published epidemiological studies.
In this, and in related studies (Neuroscience Letters, 2009, 455:173-7), we investigated the effect of continuous exposure to a global system for mobile telecommunications (GSM) modulated 900MHz signal on in vitro neuronal systems, with the specific aim to investigate if exposure to RF-EMF might act as co-stressor of well known neurotoxic agents.
We believe that co-administration of potential stressors is still a poorly explored field for both bioelectromagnetism and biology of neurodegenerative diseases. Therefore, we based our approaches to the exposure of cell systems to well-established chemical neurotoxic challengers together with RF-EMF. In order to compare the co-stressor effect on cell populations which differ in vulnerability to chemical neurotoxic challengers, we also used more than one neuronal in vitro system. We investigated beta-amyloid toxicity, as a model for AD, glutamate toxicity, as a model for excitoxic lesion operating in many conditions, and H2O2 toxicity, as a model for oxidative stress. The studies have been carried out in a SN56 cholinergic cell line and in rat primary cortical neurons. In vitro continuous exposure to 900MHz GSM–EMF guaranteed an average SAR of 1W/kg.
Compared to other studies focused on neural in vitro systems, we used a highly controlled exposure system provided with specific software to guarantee blind experiments, continuous monitoring and feedback regulation of net power and recording of all exposure and temperature data. RF exposure affected neither proliferation in control culture nor cell death due to glutamate or 25-35 beta-amyloid fragment. On the contrary, cell death rate due to oxidative stress (H2O2) was increased by RF co-exposure in SN56 cells, but not in primary neurons. Cholinergic neurons derived from the medial septum as SN56 cells, are intrinsically more sensitive than primary cortical neurons to nitric oxide excess, which is induced by in vitro culturing. These data support the view that oxidative stress might be the underlying mechanism responsible for the reported cellular effects of RF radiation. They also indicate that RF radiation could be dangerous in selected conditions and on specific neuronal populations.