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

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
• oxidative stress
• lung
• oxygen
• acute lung injury

Acknowledgements

National Council for Scientific and Technological Development (Conselho Nacional de Desenvolvimento Científico e Tecnológico -CNPq).

Authors’ contributions

LT and FP conceived, designed, and coordinated the experiments and manuscript preparation. LT, RSM and LJ performed the hyperoxia induction. LGD and FFG performed the oxidative stress analyses. NAE, MRS and GTR performed the mitochondrial respiratory chain analyses. SB and NP performed the histological analyze. RWQ, KM and FP analyzed the data, prepared the figures, and wrote the manuscript. FP revised and edited the manuscript.

Consent for publication

All authors gave their consent for publication.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The data that support the findings of this study are available from the corresponding author, FP, upon reasonable request.

Additional information

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.