Adaptive response: stimulated DNA repair or decreased damage fixation?

Abstract

The aim was to review the present state of knowledge on the adaptive response and attempt to redefine the acknowledged model in the framework of the transcription-based model of damage fixation of Radford (2002). Data are reviewed that suggest that the priming stimulus is the source of signalling that eventually leads to expression of the adaptive response. For a certain time, the ‘primed’ cell can then respond to the challenge dose by an increased recovery, as compared with the control one. An essential part of the adaptive response is generation or receipt and transmission of a signal that is the direct cause of initiation of a cellular response that diminishes the effects of DNA damage. The often accepted view that DNA repair is stimulated in the ‘primed’ and challenged cell is not supported by all the available data. Taking into account the abrogation of radio-adaptation by poly(ADP-ribosylation) inhibitors applied simultaneously with the challenge dose and the fact that adaptation is revealed as a decrease in chromosomal aberration frequency, one can apply to the adaptive response the same arguments as those that support the fixation model of Radford. Adaptive response (at least in part) is due to diminished fixation of double-strand breaks in the transcription factories by the mechanism proposed by Radford.

• Adaptive response
• DNA damage fixation model of Radford
• double strand breaks
• poly(ADP-ribosylation)