The results of numerous studies indicate that cells can become refractory t
o the detrimental effect of ionizing radiation when previously exposed to a
low, "adapting dose". This phenomenon has been termed an "adaptive respons
e" to ionizing radiation. It has been postulated that the induced radioresi
stance is due to the induction of DNA repair systems which efficiently prot
ect the adapted cells from the effects of a subsequent, high "challenging d
ose". However, a direct proof of this hypothesis is still lacking. The anal
yzed endpoints include chromosomal aberrations, survival, mutations, geneti
c instability and DNA damage repair measured by the comet assay. Frequently
contradictory results were published by different authors. For example som
e authors observed a reduced frequency of apoptosis in adapted cells, where
as others reported the opposite. The source of variablity of the adaptive r
esponse in human lymphocytes remains unresolved. While there is no doubt th
at an adapting dose can trigger some protecting mechanisms within the cell
it appears that there is no single, universal mechanism of the adaptive res
ponse that is valid for all cell, types and irradiation conditions.