| Magnetic-Field-Induced DNA Strand Breaks in Brain Cells of the Rat Henry Lai and Narendra P. Singh Bioelectromagnetics Research Laboratory, Department of Bioengineering, University of Washington, Seattle, Washington, USA Abstract
In previous research, we found that rats acutely (2 hr) exposed to a 60-Hz sinusoidal magnetic field at intensities of 0.1-0.5 millitesla (mT) showed increases in DNA single- and double-strand breaks in their brain cells. Further research showed that these effects could be blocked by pretreating the rats with the free radical scavengers melatonin and N-tert-butyl- -phenylnitrone, suggesting the involvement of free radicals. In the present study, effects of magnetic field exposure on brain cell DNA in the rat were further investigated. Exposure to a 60-Hz magnetic field at 0.01 mT for 24 hr caused a significant increase in DNA single- and double-strand breaks. Prolonging the exposure to 48 hr caused a larger increase. This indicates that the effect is cumulative. In addition, treatment with Trolox (a vitamin E analog) or 7-nitroindazole (a nitric oxide synthase inhibitor) blocked magnetic-field-induced DNA strand breaks. These data further support a role of free radicals on the effects of magnetic fields. Treatment with the iron chelator deferiprone also blocked the effects of magnetic fields on brain cell DNA, suggesting the involvement of iron. Acute magnetic field exposure increased apoptosis and necrosis of brain cells in the rat. We hypothesize that exposure to a 60-Hz magnetic field initiates an iron-mediated process (e.g., the Fenton reaction) that increases free radical formation in brain cells, leading to DNA strand breaks and cell death. This hypothesis could have an important implication for the possible health effects associated with exposure to extremely low-frequency magnetic fields in the public and occupational environments. Key words: apoptosis, DNA strand breaks, free radicals, iron, magnetic field, necrosis. Environ Health Perspect 112:687-694 (2004) . doi:10.1289/ehp.6355 available via http://dx.doi.org/ [Online 27 January 2004]
Address correspondence to H. Lai, Department of Bioengineering, Box 357962, University of Washington, Seattle, WA 98195-7962 USA. Telephone: (206) 543-1071. Fax: (206) 685-3925. E-mail: hlai@u.washington.edu Research reported in this paper was supported by the National Institute of Environmental Health Sciences (grants ES-06290 and ES-08865) . The authors declare they have no competing financial interests. Received 25 March 2003 ; accepted 27 January 2004.
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