Ferroptosis plays an important role in promoting ionizing radiation-induced intestinal injuries

Biochem Biophys Res Commun. 2022 Mar 5:595:7-13. doi: 10.1016/j.bbrc.2022.01.068. Epub 2022 Jan 21.

Abstract

The intestinal tract is an essential component of the body's immune system, and is extremely sensitive to exposure of ionizing radiation. While ionizing radiation can effectively induce multiple forms of cell death, whether it can also promote ferroptosis in intestinal cells and the possible interrelationship between ferroptosis and intestinal immune function has not been reported so far. Here, we found that radiation-induced major ultrastructural changes in mitochondria of small intestinal epithelial cells and the changes induced in iron content and MDA levels in the small intestine were consistent with that observed during cellular ferroptosis, thus suggesting occurrence of ferroptosis in radiation-induced intestinal damage. Moreover, radiation caused a substantial increase in the expression of ferroptosis-related factors such as LPCAT3 and ALOX15 mRNA, augmented the levels of immune-related factors INF-γ and TGF-β mRNA, and decreased the levels of IL-17 mRNA thereby indicating that ionizing radiation induced ferroptosis and impairment of intestinal immune function. Liproxstatin-1 is a ferroptosis inhibitor that was found to ameliorate radiation-induced ferroptosis and promote the recovery from immune imbalances. These findings supported the role of ferroptosis in radiation-induced intestinal immune injury and provide novel strategies for protection against radiation injury through regulation of the ferroptosis pathway.

Keywords: Ferroptosis; Immune; Intestinal; Ionizing radiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Acylglycerophosphocholine O-Acyltransferase / genetics
  • 1-Acylglycerophosphocholine O-Acyltransferase / metabolism
  • Animals
  • Arachidonate 12-Lipoxygenase / genetics
  • Arachidonate 12-Lipoxygenase / metabolism
  • Arachidonate 15-Lipoxygenase / genetics
  • Arachidonate 15-Lipoxygenase / metabolism
  • Ferroptosis / drug effects
  • Ferroptosis / physiology*
  • Ferroptosis / radiation effects
  • Gene Expression / drug effects
  • Gene Expression / radiation effects
  • Glutathione / metabolism
  • Intestine, Small / drug effects
  • Intestine, Small / metabolism
  • Intestine, Small / radiation effects
  • Intestines / drug effects
  • Intestines / pathology*
  • Intestines / radiation effects
  • Male
  • Malondialdehyde / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Microscopy, Electron, Transmission
  • Mitochondria / drug effects
  • Mitochondria / radiation effects
  • Mitochondria / ultrastructure
  • Quinoxalines / pharmacology*
  • Radiation Injuries, Experimental / pathology
  • Radiation Injuries, Experimental / physiopathology
  • Radiation Injuries, Experimental / prevention & control*
  • Radiation, Ionizing*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Spiro Compounds / pharmacology*
  • Superoxide Dismutase / metabolism

Substances

  • Quinoxalines
  • Spiro Compounds
  • liproxstatin-1
  • Malondialdehyde
  • Alox15 protein, mouse
  • Arachidonate 12-Lipoxygenase
  • Arachidonate 15-Lipoxygenase
  • Superoxide Dismutase
  • 1-Acylglycerophosphocholine O-Acyltransferase
  • LPCAT3 protein, mouse
  • Glutathione