ABSTRACT
Exposure to a power-frequency magnetic field has been reported to produce a statistically significant inhibition of gap junctional communication (GJC) in Clone 9 cells that have been pre-stressed by treatment with low concentrations of chloral hydrate (CH) [C.F. Blackman, J.P. Blanchard, S.G. Benane, D.E. House, J.A. Elder, Double blind test of magnetic field effects on neurite outgrowth, Bioelectromagnetics, 19 (1998) 204-209]. This observation might provide mechanistic insight into the possible role of electromagnetic fields (EMFs) in the carcinogenic process, since cancer cells frequently show decreased or absent GJC, and tumor promoting chemicals have been observed to inhibit GJC. Magnetic field exposure conditions were 45 Hz, 23.8 microT rms + parallel DC 36.6 microT, for 30 min of exposure. The responses of Clone 9 cells to the GJC-inhibiting effects of the tumor promoter 12-O-tetradecanoylphorbol 13-acetate and the chemical CH were evaluated and compared to reported results [S.G. Benane, C.F. Blackman, D.E. House, Effects of perchloroethylene and its metabolites on intercellular communication in Clone 9 rat liver cells, J. Toxicol. Environ. Health, 48 (1996) 427-437]. Before magnetic field exposure, cells were exposed for 24 h to either 3 (nine experiments) or 5 mM (11 experiments) CH to produce GJC of 67% or 50%, respectively, relative to unexposed controls. GJC was assessed microscopically using the scrape-loading technique and a blinded protocol. No statistically significant effect was observed due to magnetic field exposure with either CH concentration.
