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1 May 2000 60 Hz Magnetic Fields Do Not Enhance Cell Killing by Genotoxic Chemicals in Ataxia Telangiectasia and Normal Lymphoblastoid Cells
Lise I. Loberg, Melissa J. Luther, James R. Gauger, David L. McCormick
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Abstract

Loberg, L. I., Luther, M. J., Gauger, J. R. and McCormick, D. L. 60 Hz Magnetic Fields Do Not Enhance Cell Killing by Genotoxic Chemicals in Ataxia Telangiectasia and Normal Lymphoblastoid Cells.

Ataxia telangiectasia (AT) is an inherited autosomal recessive disease characterized by increased risk of cancer, immune deficiency, and neurodegeneration. Cells cultured from AT patients are highly sensitive to genotoxic agents and are deficient in cell cycle arrest after exposure to ionizing radiation. In consideration of their sensitivity to both ionizing and nonionizing radiation, AT cells may provide a sensitive model system to study the biological activity of other components of the electromagnetic spectrum. To characterize the effects of power-frequency (60 Hz) magnetic fields (MFs) in AT cells, we compared responses of AT and normal lymphoblast cells to sinusoidal MFs at 1.0 mT, either alone or in combination with the genotoxic agents mitomycin C or streptonigrin. The MF alone had no effect on cell growth or survival in a clonogenic assay in either AT or normal cells. The MF also had no effect on induction of cell death by mitomycin C or streptonigrin in either cell type. AT cells do not demonstrate differential sensitivity to MF exposure. These results do not support the hypothesis that MFs interact with genotoxic agents to induce adverse biological effects in either normal or genetically susceptible human cells.

Lise I. Loberg, Melissa J. Luther, James R. Gauger, and David L. McCormick "60 Hz Magnetic Fields Do Not Enhance Cell Killing by Genotoxic Chemicals in Ataxia Telangiectasia and Normal Lymphoblastoid Cells," Radiation Research 153(5), 685-689, (1 May 2000). https://doi.org/10.1667/0033-7587(2000)153[0685:HMFDNE]2.0.CO;2
Received: 1 September 1999; Accepted: 1 January 2000; Published: 1 May 2000
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