50-Hz extremely low frequency electromagnetic fields enhance cell proliferation and DNA damage: possible involvement of a redox mechanism.
HL-60 leukemia cells, Rat-1 fibroblasts and WI-38 diploid fibroblasts were exposed for 24-72 h to 0.5-1.0-mT 50-Hz extremely low frequency electromagnetic field (ELF-EMF). This treatment induced a dose-dependent increase in the proliferation rate of all cell types, namely about 30% increase of cell proliferation after 72-h exposure to 1.0 mT. This was accompanied by increased percentage of cells in the S-phase after 12- and 48-h exposure. The ability of ELF-EMF to induce DNA damage was also investigated by measuring DNA strand breaks. A dose-dependent increase in DNA damage was observed in all cell lines, with two peaks occurring at 24 and 72 h. A similar pattern of DNA damage was observed by measuring formation of 8-OHdG adducts. The effects of ELF-EMF on cell proliferation and DNA damage were prevented by pretreatment of cells with an antioxidant like alpha-tocopherol, suggesting that redox reactions were involved. Accordingly, Rat-1 fibroblasts that had been exposed to ELF-EMF for 3 or 24 h exhibited a significant increase in dichlorofluorescein-detectable reactive oxygen species, which was blunted by alpha-tocopherol pretreatment. Cells exposed to ELF-EMF and examined as early as 6 h after treatment initiation also exhibited modifications of NF kappa B-related proteins (p65-p50 and I kappa B alpha), which were suggestive of increased formation of p65-p50 or p65-p65 active forms, a process usually attributed to redox reactions. These results suggest that ELF-EMF influence proliferation and DNA damage in both normal and tumor cells through the action of free radical species. This information may be of value for appraising the pathophysiologic consequences of an exposure to ELF-EMF.
Wolf
Federica I
FI
Institute of General Pathology and Giovanni XXIII Cancer Research Center, L.go F. Vito, 1-00168 Rome, Italy. fwolf@rm.unicatt.it
Torsello
Angela
A
Tedesco
Beatrice
B
Fasanella
Silvia
S
Boninsegna
Alma
A
D'Ascenzo
Marcello
M
Grassi
Claudio
C
Azzena
Gian Battista
GB
Cittadini
Achille
A
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology; D015153:Blotting, Western; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000528:radiation effects*; D018736:DNA Adducts; D004249:DNA Damage / Q000528:radiation effects*; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000378:metabolism; D004307:Dose-Response Relationship, Radiation; D004574:Electromagnetic Fields; D005347:Fibroblasts / Q000378:metabolism; D005434:Flow Cytometry; D005452:Fluoresceins / Q000494:pharmacology; D005609:Free Radicals; D018922:HL-60 Cells; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species; D013997:Time Factors; D024502:alpha-Tocopherol / Q000494:pharmacology
D000975:Antioxidants; D018736:DNA Adducts; D005452:Fluoresceins; D005609:Free Radicals; D016328:NF-kappa B; D017382:Reactive Oxygen Species; C037631:2',7'-dichlorofluorescein; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine; D024502:alpha-Tocopherol