Differential response induced by exposure to low-dose ionizing radiation in SHSY-5Y and normal human fibroblast cells |
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Authors: | A. McLachlan-Burgess S. McCarthy C. Griffin J. Richer R. G. Cutler S. Pandey |
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Affiliation: | (1) Department of Chemistry and Biochemistry, University of Windsor, 401 Sunset Avenue, N9B 3P4 Windsor, ON, Canada;(2) Windsor Regional Cancer Centre, Windsor, ON, Canada;(3) Kronos Science Laboratories, Phoenix, AZ |
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Abstract: | Radiation therapy has been used in the treatment of a wide variety of cancers for nearly a century and is one of the most effective ways to treat cancer. Low-dose ionizing radiation (IR) can interfere with cell division of cancer and normal cells by introducing oxidative stress and injury to DNA. The differences in the response to IR-induced DNA damage and increased reactive oxygen species between normal human fibroblasts (NHFs) and cancerous SHSY-5Y cells were considered. H2AX staining and comet assays revealed that NHF cells responded by initiating a DNA repair sequence whereas SHSY-5Y cells did not. In addition, NHF cells appeared to quench the oxidative stress induced by IR, and after 24 h no DNA damage was present. SHSY-5Y cells, however, did not repair their DNA, did not quench the oxidative stress, and showed characteristic signs that they were beginning to undergo apoptosis. These results indicate that there is a differential response between this cancerous and normal cell line in their ability to respond to low-dose IR, and these differences need to be exploited in order to treat cancer effectively. Further study is needed in order to elucidate the mechanism by which SHSY-5Y cells undergo apoptosis following radiation and why these normal cells are better equipped to deal with IR-induced double-strand breaks and oxidative stress. |
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Keywords: | Radiation apoptosis double-strand breaks DNA damage DNA repair |
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