Implications of repair models for LET effects and other radiobiological phenomena.
Repair models account for shoulders to survival curves by the postulate of a mode of repair which is depleted ("saturated") as dose increases, and which should therefore be distinguished, conceptually and linguistically, from what is commonly known as "repair of potentially lethal damage". Acceptance of repair models entails new interpretations of some radiobiological phenomena. "Recovery" of cells between dose fractions would be attributable to reconstitution or resynthesis of the putative agent of repair, so elucidation of the mechanism of such "recovery" requires a different approach from any that have been used in attempts to discover the nature of "sub-lethal lesions" or the mechanism of their repair--attempts that have not been attended by success. Even mammalian cells can yield exponential survival curves; but this fact has been ignored in some proposals for mechanisms of radiation-induced cell killing, and in "theories of RBE" based on multi-sublethal lesion models for shouldered survival curves. According to repair models, however, cells in general are basically single-hit detectors. Comparisons between the responses of repair-proficient cells and their deficient mutants to change in radiation quality support the hypothesis that increases in RBE are attributable to reduced capacity for some mode(s) of repair as LET increases; but there is evidence that some capacity remains, even at very high values of LET.
D000818:Animals; D002470:Cell Survival / Q000528:radiation effects*; D002478:Cells, Cultured; D006224:Cricetinae; D004307:Dose-Response Relationship, Radiation; D004735:Energy Transfer; D004926:Escherichia coli / Q000528:radiation effects; D006801:Humans; D051379:Mice; D008954:Models, Biological; D012062:Relative Biological Effectiveness