Journal
DNA REPAIR
Volume 11, Issue 1, Pages 12-21Publisher
ELSEVIER
DOI: 10.1016/j.dnarep.2011.10.024
Keywords
Radiation; Protein oxidation; Carbonylation; DNA double strand break (DSB) repair; Manganese (II) antioxidant complexes; Reactive oxygen species (ROS); Metabolite accumulation; Deinococcus; Archaea; Mammalian cells; Cancer cells
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Funding
- Air Force Office of Scientific Research [FA9550-07-1-0218]
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A founding concept of radiobiology that deals with X-rays, gamma-rays and ultraviolet light is that radiation indiscriminately damages cellular macromolecules. Mounting experimental evidence does not fit into this theoretical framework. Whereas DNA lesion-yields in cells exposed to a given dose and type of radiation appear to be fixed, protein lesion-yields are highly variable. Extremely radiation resistant bacteria such as Deinococcus radiodurans have evolved extraordinarily efficient antioxidant chemical defenses which specifically protect proteins and the functions they catalyze. In diverse prokaryotes, the lethal effects of radiation appear to be governed by oxidative protein damage, which inactivates enzymes including those needed to repair and replicate DNA. These findings offer fresh insight into the molecular mechanisms of radiation resistance and present themselves as new opportunities to study and control oxidative stress in eukaryotes, including mammalian cells and their cancer cell counterparts. Published by Elsevier B.V.
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