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Induction of DNA double strand breaks by arsenite: comparative studies with DNA breaks induced by X-rays

Ryuichi Okayasu1, Sentaro Takahashi, Hiroshi Sato

  • 1International Space Radiation Laboratory and Environmental Toxicological Research Group, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan. rokayasu@nirs.go.jp

DNA Repair
|January 28, 2003
PubMed

Insights

Sodium arsenite induces DNA double-strand breaks (DSBs) in Chinese hamster ovary cells. Arsenite-induced DSBs require different repair mechanisms than X-ray-induced DSBs, warranting further investigation.

Area of Science:

  • Cell Biology
  • Molecular Toxicology
  • DNA Repair Mechanisms

Background:

  • Arsenic is a toxic metalloid with known genotoxic effects.
  • DNA double-strand breaks (DSBs) are critical lesions that can lead to cell death or mutations.
  • Understanding how cells repair arsenite-induced DNA damage is crucial for assessing arsenic toxicity.

Purpose of the Study:

  • To investigate the effects of sodium arsenite on cell survival and DNA double-strand break (DSB) induction in different DNA repair-proficient and deficient Chinese hamster ovary (CHO-K1) cell lines.
  • To compare the DNA damage response to arsenite with that induced by X-rays.
  • To explore the potential involvement of specific DNA repair pathways in arsenite toxicity.

Main Methods:

  • Exposure of CHO-K1 wild-type, xrs-5 (Ku80 deficient), and irs-20 (DNA-PKcs deficient) cells to various concentrations of sodium arsenite for 2.5 hours.
  • Assessment of colony-forming ability to determine cell survival.
  • Quantification of dose-dependent DNA double-strand break (DSB) induction using appropriate assays.
  • Comparison of arsenite-induced DNA damage and cell survival with X-ray-induced effects.

Main Results:

  • Sodium arsenite exposure led to a dose-dependent induction of DNA double-strand breaks (DSBs) in all tested cell lines.
  • Cell survival varied significantly, with wild-type cells exhibiting the highest survival, xrs-5 cells the lowest, and irs-20 cells showing intermediate survival.
  • The pattern of cell survival mirrored responses to X-ray irradiation.
  • Arsenite exposure required the induction of twice as many DNA-DSBs in wild-type cells to achieve similar cell survival compared to X-rays, suggesting distinct lesion types.

Conclusions:

  • Sodium arsenite induces DNA DSBs in CHO-K1 cells, impacting cell survival.
  • The DNA damage induced by arsenite appears to involve different types of lesions or requires distinct repair pathways compared to X-ray-induced damage.
  • Further mechanistic studies focusing on DNA-DSB repair proteins are necessary to elucidate the recovery process from arsenic exposure.
Keywords:
Non-programmatic

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