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Related Concept Videos

Biological Effects of Radiation02:59

Biological Effects of Radiation

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All radioactive nuclides emit high-energy particles or electromagnetic waves. When this radiation encounters living cells, it can cause heating, break chemical bonds, or ionize molecules. The most serious biological damage results when these radioactive emissions fragment or ionize molecules. For example, α and β particles emitted from nuclear decay reactions possess much higher energies than ordinary chemical bond energies. When these particles strike and penetrate matter, they...
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Enrichment of Native and Recombinant Extracellular Vesicles of Mycobacteria
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Radiation-Resistant Bacteria Deinococcus radiodurans-Derived Extracellular Vesicles as Potential Radioprotectors.

Jeong Moo Han1,2,3,4, Godfrey Mwiti5,6, Seo-Joon Yeom1,7

  • 1Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup-si, Jeollabuk-do, 56212, Republic of Korea.

Advanced Healthcare Materials
|December 16, 2024
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Deinococcus radiodurans (R1-EVs) show significant radioprotective effects against total body irradiation (TBI)-induced acute radiation syndrome (ARS). Pretreatment with R1-EVs enhances survival rates and protects against radiation damage by scavenging reactive oxygen species (ROS).

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Deinococcus radioduransacute radiation syndromeextracellular vesiclesradioprotector

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Area of Science:

  • Radiation Biology
  • Cellular Biology
  • Microbiology

Background:

  • Radiation exposure poses health risks, necessitating the development of effective radioprotectors.
  • Deinococcus radiodurans (R1-EVs) have demonstrated antioxidative properties in prior research.
  • The radioprotective potential of R1-EVs against acute radiation syndrome (ARS) requires further investigation.

Purpose of the Study:

  • To evaluate the radioprotective effects of R1-EVs against total body irradiation (TBI)-induced ARS in a mouse model.
  • To assess the impact of R1-EVs on hematopoietic and gastrointestinal ARS.
  • To elucidate the mechanisms underlying R1-EVs' radioprotective activity.

Main Methods:

  • Mice were subjected to 8 Gy TBI to induce ARS.
  • R1-EVs were administered as a pretreatment to assess protection against radiation-induced mortality.
  • Hematopoietic (bone marrow, spleen) and gastrointestinal (intestinal stem and epithelial cells) protection was evaluated.
  • Mechanisms including reactive oxygen species (ROS) scavenging, cytokine modulation, and short-chain fatty acid production were analyzed.
  • Proteomic analysis identified proteins involved in oxidative stress response within R1-EVs.

Main Results:

  • Pretreatment with R1-EVs significantly increased survival rates in irradiated mice compared to the control group.
  • R1-EVs effectively protected bone marrow cells and splenocytes from radiation-induced death by scavenging ROS.
  • R1-EVs demonstrated protective effects on intestinal stem and epithelial cells, mitigating radiation-induced apoptosis.
  • R1-EVs modulated the gut environment by stimulating short-chain fatty acid production, suppressing proinflammatory cytokines, and increasing regulatory T cells.
  • Proteomic analysis revealed enrichment of oxidative stress response proteins in R1-EVs.

Conclusions:

  • R1-EVs exhibit potent radioprotective capabilities against TBI-induced ARS.
  • R1-EVs protect against radiation damage through ROS scavenging and modulation of the immune and gastrointestinal environments.
  • These findings suggest R1-EVs hold promise as therapeutic agents for radiation damage and ROS-related diseases.