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Intestinal microbiota reduces genotoxic endpoints induced by high-energy protons
Irene Maier1, David M Berry, Robert H Schiestl
1a Department of Environmental Health Sciences, Fielding School of Public Health, University of California, Los Angeles, California;
Radiation Research
|January 9, 2014
Summary
Mice with restricted gut microbiota (RM) showed more DNA damage after space radiation than those with conventional microbiota (CM). RM microbiota may impair DNA repair, increasing cancer risk.
Area of Science:
- Astrobiology
- Radiation Biology
- Microbiome Research
Background:
- Ionizing space radiation induces oxidative DNA damage and stress.
- Impaired DNA repair mechanisms elevate cancer risk.
- The gut microbiota's role in radiation response is under investigation.
Purpose of the Study:
- To investigate the impact of gut microbiota composition on DNA damage and repair after space radiation exposure.
- To compare the effects of different types of space radiation on mice with conventional (CM) and restricted (RM) microbiota.
Main Methods:
- Young adult mice with CM or RM were exposed to whole-body irradiation (protons, silicon, or iron ions).
- Chromosomal DNA lesions were assessed 6 hours post-irradiation.
- Gut microbiota composition was analyzed using high-throughput rRNA gene sequencing.
- DNA repair marker (γ-H2AX) and antioxidant (glutathione) levels were measured.
Main Results:
- Mice with RM exhibited acute chromosomal DNA lesions, unlike CM mice.
- Specific bacterial phylotypes (Barnesiella intestinihominis, unclassified Bacterodiales) were more abundant in male RM mice.
- RM mice exposed to protons showed elevated γ-H2AX phosphorylation and decreased glutathione.
- CM mice displayed lower γ-H2AX levels and shifts in RM-associated phylotypes post-irradiation.
Conclusions:
- Restricted gut microbiota composition exacerbates DNA damage and impairs DNA repair following space radiation.
- Specific microbial alterations in RM mice correlate with increased radiosensitivity.
- Gut microbiota modulation may be a strategy to mitigate radiation-induced carcinogenesis.
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