Induction of chromatid breaks by carbon K-shell ultrasoft X rays

Radiat Res. 2003 Feb;159(2):247-50. doi: 10.1667/0033-7587(2003)159[0247:iocbbc]2.0.co;2.

Abstract

Chromatid breaks have previously been shown to be induced in G2-phase cells after exposure to ionizing radiation (X and gamma rays) as a linear function of dose, consistent with a single-event mechanism. DNA double-strand breaks (DSBs) are thought to be the initiating lesion, and experiments with a genetically engineered cell line containing a single DSB site also indicate that a single DSB is sufficient to induce a chromatid break. Although the precise mechanism of conversion of an isolated DSB into a chromatid break is not yet understood, it is known that a proportion of chromatid breaks result from rearrangements between sister chromatids. Here we report further evidence for the single-event hypothesis for the formation of chromatid breaks. The evidence derives from experiments in which chromatid breaks have been induced by exposure of Chinese hamster cells to ultrasoft carbon K-shell X rays. Since the energy of carbon K-shell X rays is not sufficient for the secondary electrons to span more than one DNA double helix, we conclude that single traversals, and hence single (complex) DSBs, are responsible for the formation of chromatid breaks. We find that, as for 60Co gamma rays, around 10% of the carbon K-shell X-ray-induced chromatid breaks have associated color switches at breakpoints, indicating that they arise through sister chromatid rearrangements.

MeSH terms

  • Animals
  • CHO Cells
  • Carbon / chemistry*
  • Chromatids / drug effects
  • Chromatids / genetics
  • Chromatids / metabolism
  • Chromatids / radiation effects*
  • Cobalt Radioisotopes / chemistry
  • Cricetinae
  • DNA Damage / drug effects
  • DNA Damage / radiation effects*
  • Gamma Rays
  • Metaphase / radiation effects
  • Radiometry
  • X-Rays*

Substances

  • Cobalt Radioisotopes
  • Carbon