DNA damage as the cause of ionizing radiation-induced gene activation.

Tyrosine kinases have been shown to be activated by both UVA and UVC light and gamma irradiation. For UV exposure, a non-DNA target has been proposed. Here the possibility of a non-DNA target for ionizing radiation is examined. A comparison of the fluence/dose to which the cells were exposed to elicit the response indicates that three orders of magnitude greater numbers of potentially damaging events occur after UVC exposure than after gamma irradiation. Thus, while the involvement of a non-DNA target by UVC is possible, the probability of "hits" on such targets by ionizing radiation events is remote. The levels of intracellular endogenous oxidation damage are compared to those produced by ionizing radiation. This indicates that an oxidation product which is rapidly repaired and which is therefore present at low endogenous levels, such as the DNA single-strand break, is a candidate lesion for signal induction.

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