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Related Concept Videos

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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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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Related Experiment Video

Updated: Feb 17, 2026

Intestinal Epithelial Regeneration in Response to Ionizing Irradiation
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Cobalt Chloride Protects Against Intestinal Irradiation-Induced Injury by Activating the HIF-2α.

Jianpeng Zhao1, Ruling Liu1, Zhaoyong Shou2

  • 1Faculty of Naval Medicine, Naval Medical University, Shanghai, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|February 16, 2026
PubMed
Summary

Cobalt chloride (CoCl2) pretreatment significantly improves survival and intestinal integrity after radiation exposure. It protects against radiation injury by promoting cell proliferation and enhancing barrier function via hypoxia-inducible factor-2α (HIF-2α).

Keywords:
CoCl2HIF‐2αPHD‐HIF signaling pathwayradiation injuryradiation protectionradiation‐induced intestinal injury

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Area of Science:

  • Radiation biology
  • Medical countermeasures
  • Nuclear medicine

Background:

  • Geopolitical instability increases the risk of nuclear incidents, potentially causing widespread acute radiation injury.
  • Intestinal radiation sickness is a severe consequence of high-dose ionizing radiation (IR).
  • Effective radioprotective agents are crucial for mitigating radiation-induced damage.

Purpose of the Study:

  • To investigate the protective effects of cobalt chloride (CoCl2) against intestinal radiation injury.
  • To elucidate the preliminary mechanisms underlying CoCl2's radioprotective action.
  • To provide a scientific basis for developing novel radiation protection strategies.

Main Methods:

  • In vitro studies using cells and intestinal organoids.
  • In vivo studies using live mice models.
  • Assessment of survival rates, intestinal injury scores, villi structure, cell apoptosis, gene expression, and hypoxia-inducible factor-2α (HIF-2α) signaling.

Main Results:

  • CoCl2 pretreatment significantly enhanced radiation tolerance and survival rates in mice.
  • It preserved intestinal villi structure, promoted organoid proliferation, inhibited apoptosis, and boosted barrier protection gene expression.
  • Mechanism analysis revealed CoCl2 up-regulates HIF-2α, activating downstream pathways for proliferation, anti-apoptosis, and angiogenesis.

Conclusions:

  • CoCl2 demonstrates significant radioprotective effects against intestinal radiation injury.
  • The protective mechanism involves HIF-2α activation, enhancing cellular resilience and tissue integrity.
  • CoCl2 offers a promising strategy for developing new radioprotective agents for nuclear radiation protection.