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

  • Leonardo Tenfen
  • , Richard Simon Machado
  • , Khiany Mathias
  • , Natalia Piacentini
  • , Larissa Joaquim
  • , Sandra Bonfante
  • , Lucineia Gainski Danielski
  • , Nicole Alessandra Engel
  • , Mariella Reinol da Silva
  • , Gislaine Tezza Rezin
  • , Rafaella Willig de Quadros
  • , Fernanda Frederico Gava
  • , Fabricia Petronilho

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)174-188
Number of pages15
JournalInhalation toxicology
Volume36
Issue number3
DOIs
StatePublished - 2024
Externally publishedYes

Keywords

  • acute lung injury
  • Hyperoxia
  • lung
  • oxidative stress
  • oxygen

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

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