Cytostatic response of NB69 cells to weak pulse-modulated 2.2 GHz radar-like signals
Article first published online: 28 JAN 2011
Copyright © 2011 Wiley-Liss, Inc.
Volume 32, Issue 5, pages 340–350, July 2011
How to Cite
Trillo, M. A., Cid, M. A., Martínez, M. A., Page, J. E., Esteban, J. and Úbeda, A. (2011), Cytostatic response of NB69 cells to weak pulse-modulated 2.2 GHz radar-like signals. Bioelectromagnetics, 32: 340–350. doi: 10.1002/bem.20643
- Issue published online: 23 MAY 2011
- Article first published online: 28 JAN 2011
- Manuscript Accepted: 2 DEC 2010
- Manuscript Received: 3 MAY 2010
- Spanish Ministry of Defence (Radiofrequency Biological Effects). Grant Number: MOU EUROPA ERG 101.013
- radiofrequency radiation;
- cell proliferation;
- cell cycle
The present study investigates the response of two human cancer cell lines to a 24-h treatment with a 2.2-GHz, pulse-modulated (5 µs pulse duration, 100 Hz repetition rate) radar-like signal at an average SAR = 0.023 W/kg, using a newly designed setup for in vitro exposure to radiofrequency (RF) fields. A complete discretized model of the setup was created for numerical dosimetry using finite-difference time-domain (FDTD) software, SEMCAD X. The average dose of RF radiation absorbed by the cultures was calculated to be subthermal (ΔT < 0.1 °C). The RF exposure induced a consistent, statistically significant reduction in the cell number (13.5% below controls, P < 0.001) in the neuroblastoma NB69 line. This effect was accompanied with slight but statistically significant increases in the proportions of cells in phases G0/G1 and G2/M of the cell cycle (6% and 9%, respectively; P < 0.05 over controls). By contrast, the hepatocarcinoma cell line HepG2 did not respond to the same RF treatment. These results indicate that a pulse-modulated RF radiation with high instantaneous amplitude and low average power can induce cytostatic responses on specific, sensitive cancer cell lines. The effect would be mediated, at least in part, by alterations in the kinetics of the cell cycle. Bioelectromagnetics 32:340–350, 2011. © 2010 Wiley-Liss, Inc.