[Hypersensitivity following low one-time irradiation dosage and induced radio resistance]

There is now little doubt of the existence of radioprotective mechanisms, or stress responses, that are upregulated in response to exposure with small doses of ionizing radiation and other DNA-damaging agents. Phenomenologically, there are two ways in which these induced mechanisms operate. First, a small conditioning dose (generally below 30 cGy) may protect against a subsequent, separate irradiation. This has been termed the adaptive response. Second, the response to single doses may itself be dose-dependent so that small acute radiation exposures are more effective per unit dose than larger exposures above the threshold where the induced radioprotection is triggered. This combination has been termed low dose hypersensitivity (HRS) and induced radioresistance (IRR) as the dose increases. Both the adaptive response and HRS/IRR have been well documented in studies with yeast, bacteria, protozoa, algae, higher plant cells, insect cells, mammalian and human cells in vitro, and in studies on animal models in vivo. There is indirect evidence that the adaptive response and the IRR phenomenon in response to single doses is a manifestation of the same underlying mechanisms, namely an increase of the amount and rate of DNA repair induced by low radiation doses.