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Updated: May 29, 2026

Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation
Published on: July 3, 2015
[Radiation adaptive response as a stress reaction of a cell]
Abstract:
The published data on the primary changes that occur in human peripheral blood lymphocytes after small dose irradiation in vitro (SDI), as well as relation between these changes and the adaptive response mechanism (increase of radioresistance of lymphocytes after SDI) have been analyzed. The author has come to a conclusion in favor of the absence among the revealed primary changes of any traces of a specific inducible mechanism that protects a cell from exterior influences and elevates cell radioresistance. The changes in cell radioresistance following the SDI comprise only an insignificant part of all the changed characteristics. There are large numbers of mechanisms by which radioresistance changes and they are poorly studied at that. The author speculates that the adaptive response isn't a specific radiobiological protective phenomenon, but it is rather a type of the cell stress reaction that is evoked by external influences. Signals that trigger transition to a state of stress, as well as the signals to implement adaptive functions, thus restoring the normal state, can be represented, for example, by increased concentrations of reactive oxygen species, and most likely by as yet unknown metabolic changes. An irradiated cell transfers into the state of stress and mobilizes all possible ways to increase resistance to any damaging effects, radiation including. What particular way of increasing radioresistance will be used depends on the genotype, experiment conditions, etc. The consequences of stress could cause more rapid cell division, malignant transformations and increased stability of malignization, hormesis and many other things.
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