Biological Impact of Low Dose Radiation on Mitochondrial Defective Lymphoblastoid Cells

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Environmental and Molecular Mutagenesis



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The mitochondria are key organelles important in ensuring homeostasis following radiation exposure and in mediating non-targeted effects. Radiation results in an increase in ROS and can be further enhanced in cells with damaged mitochondria, inducing persistent damage and genomic instability, which may promote cancer. Mitochondrial DNA (mtDNA), due to its less efficient repair as compared to nuclear DNA, is more severely affected by radiation exposures. All mtDNA genes are essential and these mutations often cause a deficiency in energy metabolism, thus increasing ROS and leading to oxidative stress. How these mitochondrial mutations may impact the biological response of the cell to a low dose of ionizing radiation is however unclear. In this study we investigated the kinetics of DNA damage and telomere length changes in cells with known mitochondrial mutations following a low dose (0.5 Gy) of Xray or 1 GeV/um Fe ion. Results reveal differences based on the mitochondrial mutation, endpoint assayed, and radiation quality. Results indicate that ionizing radiation of lymphoblastoid cells with mitochondrial mutations aberrantly affects DNA damage kinetics and telomere length as compared to controls and may have long-term consequences on the ability of these cells to regain homeostasis. The results of this work may provide a better understanding for the persistent genomic instability following a low dose of radiation and the changes which lead to cancer imitation or promotion.


Cell Biology



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