Re-consideration of the mechanism of adaptive response to radiation

The first priming irradiation (PI) causes radio-resistance (RR) to the second challenging irradiation (CI) in cultured cells and even in the intact animal like a mouse, which is called adaptive radio-response (AR). Recent findings on AR are: PI has a specific dose range, there is a specific time interval between PI and CI, chemical stimulation can act as either PI or CI, and stimulation and response seem to cross-talk. For these, syntheses of RNA and protein are necessary and tumor-suppressing gene p53 is found to concern as a genetic background. Along with above recent progress, AR is re-considered and discussed in this paper together with authors' findings. Apoptosis is induced in cells by CI after continuous low-dose PI, but not in p53-deleted or -mutated cells. The interval for AR between PI and CI is found as short as 48 hr: the memory of PI has a time limit. The memorizing time of PI exposure is found to be regulated by the expression of Hdm2 and p53: the feed-back control of p53 by Hdm2 is a cellular memory mechanism of radiation exposure. There are three theories for the mechanism of RR: production of radical scavenger by PI, stimulation by PI of repair mechanism like enzymes concerned, and cessation of cell cycle to make the repair easy. Authors, in their experiments using p53-deleted or -mutated cells, have found that PI induces Hdm2 to reduce p53, where NO radical is produced by CI, and thus cells obtain RR to suppress the radiation-induced chromosome aberration. These investigations on AR will help studies of radiation protection. (R.T.)