Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats

Inhal Toxicol. 2024 Mar;36(3):174-188. doi: 10.1080/08958378.2024.2322497. Epub 2024 Mar 6.

Abstract

Background: Oxygen therapy is an alternative for many patients with hypoxemia. However, this practice can be dangerous as oxygen is closely associated with the development of oxidative stress.

Methods: Male Wistar rats were exposed to hyperoxia with a 40% fraction of inspired oxygen (FIO2) and hyperoxia (FIO2 = 60%) for 120 min. Blood and lung tissue samples were collected for gas, oxidative stress, and inflammatory analyses.

Results: Hyperoxia (FIO2 = 60%) increased PaCO2 and PaO2, decreased blood pH and caused thrombocytopenia and lymphocytosis. In lung tissue, neutrophil infiltration, nitric oxide concentration, carbonyl protein formation and the activity of complexes I and II of the mitochondrial respiratory chain increased. FIO2 = 60% decreased SOD activity and caused several histologic changes.

Conclusion: In conclusion, we have experimentally demonstrated that short-term exposure to high FIO2 can cause oxidative stress in the lung.

Keywords: Hyperoxia; acute lung injury; lung; oxidative stress; oxygen.

MeSH terms

  • Animals
  • Electron Transport
  • Humans
  • Hyperoxia* / complications
  • Hyperoxia* / metabolism
  • Lung / metabolism
  • Male
  • Oxidative Stress
  • Oxygen
  • Rats
  • Rats, Wistar

Substances

  • Oxygen