The field of radiobiology is built on the premise that radiation is dangerous because of its damaging effects on DNA. Contrary to that view, Daly et al. report that the ability of cells to survive radiation is highly dependent on the amount of protein damage caused during irradiation. Surprisingly, a dose of radiation that is sufficient to cause only minor DNA damage in radiation-sensitive cells will cause high levels of protein damage compared to resistant cells exposed to the same dose.
This new model of radiation toxicity shifts the emphasis away from DNA damage toward protein damage, where DNA repair-related proteins in sensitive cells are devastated by radiation long before DNA is significantly damaged. In contrast, repair enzymes in extremely resistant cells survive and function with great efficiency after irradiation because they are protected, specifically by a chemical mechanism involving manganese (II) ions.
The new model of extreme radiation resistance reconciles many seemingly conflicting results published over the last two decades, and points directly at the existence of potent manganese-based radioprotectors that prevent protein damage. Daly expects that delivery of purified radioprotective Mn-complexes into sensitive cell-types will make them temporarily radiation resistant. This possibility opens up new avenues for radioprotection, including approaches to facilitate recovery from short- or long-term exposures to radiation such as cancer therapies, accident- or terror-related nuclear events, and astronauts exposed to cosmic radiation.
Andrew Hyde | alfa
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