The hypothesis investigated is that exposure of a mammalian cell to high peak power pulsed RF, at the frequency of 8.2 GHz, can result in the activation of an important eukaryotic transcriptional regulator, nuclear factor kappa B (NF-kappaB). This DNA-binding protein controls genes involved in long term cellular regulation. The selection of 8.2 GHz was based on the availability of a high peak power pulsed RF transmitter. In these studies, triplicate cultures of human monocytes (Mono Mac-6) were exposed to the pulsed wave radiation. The peak to average power ratio was 455:1 (2.2 micros pulse width and pulse repetition rate of 1000 pulses/s). The average power density at the position of exposure was 50 W/m(2), and the mean SAR at the bottom of the culture flask was 10.8 +/- 7.1 W/kg. The FDTD analysis indicated that 10% of the cells had an SAR of 22-29 W/kg. The cells were exposed continuously for 90 min at 37 degrees C, reincubated at this temperature, and harvested 4 h postexposure. The nuclear extracts were analyzed by electrophoretic mobility shift assay. The results showed a profound increase (3.6-fold) in the DNA binding activity of NF-kappaB in monocytes at 4 h after the pulsed RF exposure compared to sham irradiated controls. Competition experiments with cold NF-kappaB- specific oligonucleotides confirmed the specificity of the DNA binding activity. These results provide evidence that high peak power pulsed radiofrequency radiation can perturb the cell and initiate cell signaling pathways. However, at this point, we are not prepared to advocate that the cause is a nonthermal mechanism. Because of the broad distribution of SAR's in the flask, experiments need to be performed to determine if the changes observed are associated with cells exposed to high or low SARs.
Copyright 2002 Wiley-Liss, Inc.