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Updated: Nov 11, 2025

Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation
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Total body irradiation causes a chronic decrease in antioxidant levels.

Lue Sun1, Yohei Inaba2,3, Yu Sogo4

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Long-term exposure to ionizing radiation chronically reduces antioxidant capacity in mice. Glutathione levels and ratios are sensitive markers for radiation exposure, potentially contributing to late radiation effects.

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Area of Science:

  • Radiation biology
  • Oxidative stress research
  • Biomarker discovery

Background:

  • Ionizing radiation causes acute syndromes and increases long-term health risks.
  • Chronic oxidative stress is hypothesized to mediate radiation's late effects.
  • Long-term changes in antioxidant capacity post-irradiation require further investigation.

Purpose of the Study:

  • To investigate long-term changes in whole-blood antioxidant capacity and red blood cell (RBC) glutathione levels after X-ray total body irradiation (TBI) in mice.
  • To identify sensitive biomarkers for radiation exposure beyond 100 days post-irradiation.
  • To explore the link between chronic antioxidant reduction and the pathogenesis of late radiation effects.

Main Methods:

  • Male C57BL/6J mice were exposed to varying doses of X-ray TBI.
  • Whole-blood antioxidant capacity and RBC glutathione (reduced glutathione [GSH] and oxidative glutathione [GSSG]) levels were measured at ≥100 days post-TBI.
  • Complete blood counts (CBC) were also analyzed for comparison.

Main Results:

  • Whole-blood antioxidant capacity was chronically decreased in mice exposed to 5 Gy TBI.
  • RBC GSH levels and the GSH/GSSG ratio were chronically decreased after ≥1 Gy TBI.
  • GSH and the GSH/GSSG ratio showed greater sensitivity to radiation exposure than CBC counts.

Conclusions:

  • Chronic reduction in antioxidant capacity, particularly GSH levels and the GSH/GSSG ratio, persists long after radiation exposure.
  • GSH and the GSH/GSSG ratio are sensitive biomarkers for assessing long-term radiation exposure.
  • These findings support the hypothesis that chronic antioxidant depletion contributes to the development of late radiation-induced diseases.