Intracellular stimulation of biochemical control mechanisms by low-dose, low-LET irradiation.
Non-specific generation of intracellular free radicals in excess of normal levels, e.g. by the acute radiation absorption event in cells, has led to a delayed and temporary inhibition of thymidine kinase. The enzyme activity reaches a minimum at 4 h even after a low-level exposure with full recovery soon thereafter. This process appears to represent a biochemical response to an initial physical event, but must be distinguished from the response of the DNA repair enzyme system. A reduction of cellular thymidine kinase activity is expected to cause a temporary reduction of DNA synthesis and may be of advantage to the cell. Such a response may be regarded as an instance of radiation hormesis in the sense that such a compensatory response to the stimulus of irradiation may confer protection against a repeated increase in free radical concentration whether by renewed radiation exposure or by metabolism in general. An improvement of the efficiency of repair or an increased level of free radical detoxification should be of benefit to both the individual cell and to the organism as a whole.
D000818:Animals; D002477:Cells / Q000378:metabolism / Q000528:radiation effects*; D004247:DNA / Q000378:metabolism; D004307:Dose-Response Relationship, Radiation; D005609:Free Radicals; D008280:Magnetics; D051379:Mice; D013937:Thymidine Kinase / Q000378:metabolism
D005609:Free Radicals; D004247:DNA; D013937:Thymidine Kinase