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Related Experiment Videos

Adaptive response and induced resistance.

M C Joiner1, P Lambin, B Marples

  • 1Gray Laboratory Cancer Research Trust, Mount Vernon Hospital, Northwood, Middx, UK. joiner@graylab.ac.uk

Comptes Rendus De L'Academie Des Sciences. Serie III, Sciences De La Vie
|April 10, 1999
PubMed
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Cellular stress responses show low-dose hypersensitivity (HRS) and induced radioresistance (IRR), meaning low radiation doses are more lethal per unit dose. This phenomenon, observed across many species, suggests a threshold dose-risk relationship for radiation exposure.

Area of Science:

  • Radiation biology
  • Cellular stress response
  • DNA damage and repair

Background:

  • Cellular stress responses are activated by DNA-damaging agents like radiation.
  • Radiation response is dose-dependent, with low doses exhibiting higher lethality per unit dose than higher doses.
  • Low-dose hypersensitivity (HRS) and induced radioresistance (IRR) describe this non-linear dose response.

Purpose of the Study:

  • To investigate the phenomena of low-dose hypersensitivity (HRS) and induced radioresistance (IRR) in cellular responses to radiation.
  • To explore the underlying mechanisms of HRS and IRR, particularly their relation to DNA repair.
  • To assess the implications of HRS/IRR for net cancer risk at low radiation doses.

Main Methods:

  • Review of cell-survival studies across various species (yeast, bacteria, human cells) and animal models.

Related Experiment Videos

  • Analysis of evidence linking HRS/IRR to adaptive responses and DNA repair mechanisms.
  • Examination of gene expression changes following irradiation at different doses.

    • Main Results:

    • HRS/IRR has been observed in diverse biological systems, from microbes to mammalian cells.
    • Evidence suggests HRS/IRR operates via enhanced DNA repair rather than cell-cycle modulation or apoptosis.
    • Rapid gene expression changes at low doses may underlie induced radioresistance.

    Conclusions:

    • The underlying mechanism of HRS/IRR appears to involve increased DNA repair capacity.
    • HRS/IRR suggests a threshold dose-risk relationship for radiation, potentially explaining reduced cancer risk at very low doses.
    • Further research is needed to identify the specific molecular components of this adaptive response.