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. 1984;6:137–143.

Implications of repair models for LET effects and other radiobiological phenomena.

T Alper
PMCID: PMC2149139  PMID: 6365136

Abstract

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Alper T., Moore J. L., Bewley D. K. LET as a determinant of bacterial radiosensitivity, and its modification by anoxia and glycerol. Radiat Res. 1967 Oct;32(2):277–293. [PubMed] [Google Scholar]
  2. Alper T., Moore J. L. The interdependence of oxygen enhancement ratios for 250kVp X rays and fast neutrons. Br J Radiol. 1967 Nov;40(479):843–848. doi: 10.1259/0007-1285-40-479-843. [DOI] [PubMed] [Google Scholar]
  3. Courtenay V. D., Smith I. E., Peckham M. J., Steel G. G. In vitro and in vivo radiosensitivity of human tumour cells obtained from a pancreatic carcinoma xenograft. Nature. 1976 Oct 28;263(5580):771–772. doi: 10.1038/263771a0. [DOI] [PubMed] [Google Scholar]
  4. Cox R., Masson W. K. Mutation and inactivation of cultured mammalian cells exposed to beams of accelerated heavy ions. III. Human diploid fibroblasts. Int J Radiat Biol Relat Stud Phys Chem Med. 1979 Aug;36(2):149–160. doi: 10.1080/09553007914550901. [DOI] [PubMed] [Google Scholar]
  5. Fritz-Niggli H., Büchi C., Schweizer P. Oxygen-effect as an inhibition of repair: radiation studies on excision repair deficient mei-9L1-embryos of Drosophila. Radiat Environ Biophys. 1981;19(4):265–274. doi: 10.1007/BF01324092. [DOI] [PubMed] [Google Scholar]
  6. Hahn G. M., Bagshaw M. A., Evans R. G., Gordon L. F. Repair of potentially lethal lesions in x-irradiated, density-inhibited Chinese hamster cells: metabolic effects and hypoxia. Radiat Res. 1973 Aug;55(2):280–290. [PubMed] [Google Scholar]
  7. Hesslewood I. P. DNA strand breaks in resistant and sensitive murine lymphoma cells detected by the hydroxyapatite chromatographic technique. Int J Radiat Biol Relat Stud Phys Chem Med. 1978 Nov;34(5):461–469. doi: 10.1080/09553007814551121. [DOI] [PubMed] [Google Scholar]
  8. Lehman A. R., Stevens S. The production and repair of double strand breaks in cells from normal humans and from patients with ataxia telangiectasia. Biochim Biophys Acta. 1977 Jan 3;474(1):49–60. doi: 10.1016/0005-2787(77)90213-1. [DOI] [PubMed] [Google Scholar]
  9. Petin V. G., Kabakova N. M. Rbe of densely ionizing radiation for wild-type and radiosensitive mutants of yeast. Mutat Res. 1981 Jul;82(2):285–294. doi: 10.1016/0027-5107(81)90158-5. [DOI] [PubMed] [Google Scholar]
  10. Resnick M. A., Martin P. The repair of double-strand breaks in the nuclear DNA of Saccharomyces cerevisiae and its genetic control. Mol Gen Genet. 1976 Jan 16;143(2):119–129. doi: 10.1007/BF00266917. [DOI] [PubMed] [Google Scholar]
  11. Thacker J., Stretch A., Stephens M. A. Mutation and inactivation of cultured mammalian cells exposed to beams of accelerated heavy ions. II. Chinese hamster V79 cells. Int J Radiat Biol Relat Stud Phys Chem Med. 1979 Aug;36(2):137–148. doi: 10.1080/09553007914550891. [DOI] [PubMed] [Google Scholar]
  12. Todo T., Yonei S. Inhibitory effect of membrane-binding drugs on excision repair of DNA damage in UV-irradiated Escherichia coli. Mutat Res. 1983 Apr;112(2):97–107. doi: 10.1016/0167-8817(83)90014-7. [DOI] [PubMed] [Google Scholar]
  13. Utsumi H., Elkind M. M. Potentially lethal damage versus sublethal damage: independent repair processes in actively growing Chinese hamster cells. Radiat Res. 1979 Feb;77(2):346–360. [PubMed] [Google Scholar]
  14. Utsumi H., Hill C. K., Ben-Hur E., Elkind M. M. "Single-hit" potentially lethal damage: evidence of its repair in mammalian cells. Radiat Res. 1981 Sep;87(3):576–591. [PubMed] [Google Scholar]
  15. Yatagai F., Matsuyama A. LET-dependent radiosensitivity of Escherichia coli K-12 rec and uvr mutants. Radiat Res. 1977 Jul;71(1):259–263. [PubMed] [Google Scholar]

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