There is evidence that athermal radiofrequency radiation can alter Heat Shock Protein (HSP) expression or protein phosphorylation, or alter MAP kinase signalling. Effects of long-term exposure in brain tissue due to repeated HSP perturbation (eg an inhibition of apoptosis) have been hypothesised (French et al, 2001). This study aimed to investigate the RNA expression profile (12,000 genes) and HSP family protein expression levels after either acute 1-hour or chronic 4-day intermittent exposures to simulated GSM radiation in a human primary fibroblast model. The results found minimal or no effects of GSM. Flasks were exposed to 900 MHz (217 Hz modulation) at 0.18 W/kg SAR within a Transverse Electromagnetic Mode chamber (TEM cell). Cultures rested for 2 hours before exposures. Affymetrix U95A microarray analysis of a single pilot set of experiments showed that about 40 genes were reported as upregulated >=2.5 fold in each condition. There was no evidence of altered expression of any MAPK-associated genes. Target genes reported in both conditions (CBFA2T1, ZNF148, ITGA1), and genes altered in one condition (CCS, PLEC1, BIRC5), and marginally altered HSP72 were selected for PCR analysis. No other members of the HSP family were altered. In three replicate experiments assayed by real-time PCR, six genes were either unchanged or showed randomly variable expression. However HSP72 RNA showed possible consistent slight upregulation of 1.37 +/- 0.21 in the chronic condition. Western immunoblots of HSP-60, -70, -72 and -V90 proteins showed no significant changes 5 hours after exposure. In preliminary studies using a serum starvation protocol, ERK-1 phosphorylation was unaltered after 5 or 30 minutes GSM (single experiments). When flasks were transiently cooled, ERK-1 phosphorylation was increased 20 minutes later, indicating a source of artefact in some protocols. An inflammatory challenge experiment with a low-dose of the cytokine IL-1???? found that acute GSM exposure post-challenge inhibited NF????B-mediated GRO???? induction by 1.5 fold (2 experiments). Preconditioning with mild heat induces transient inhibition of both NF????B signalling and apoptosis. Other studies indicate that EMF exposures similarly evoke cytoprotection. It is suggested that GSM evoked cytoprotective signalling in this inflammatory model.
| Identifer | oai:union.ndltd.org:ADTP/215831 |
| Date | January 2005 |
| Creators | Blood, Alan, Physics, Faculty of Science, UNSW |
| Publisher | Awarded by:University of New South Wales. School of Physics |
| Source Sets | Australiasian Digital Theses Program |
| Language | English |
| Detected Language | English |
| Rights | Copyright Alan Blood, http://unsworks.unsw.edu.au/copyright |
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