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

doi:10.1080/08958378.2024.2322497

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 journal › Article › peer-review

1 Scopus citations

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 language	English (US)
Pages (from-to)	174-188
Number of pages	15
Journal	Inhalation toxicology
Volume	36
Issue number	3
DOIs	https://doi.org/10.1080/08958378.2024.2322497
State	Published - 2024
Externally published	Yes

Keywords

acute lung injury
Hyperoxia
lung
oxidative stress
oxygen

ASJC Scopus subject areas

Toxicology
Health, Toxicology and Mutagenesis

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10.1080/08958378.2024.2322497

Cite this

Tenfen, L., Simon Machado, R., Mathias, K., Piacentini, N., Joaquim, L., Bonfante, S., Danielski, L. G., Engel, N. A., da Silva, M. R., Rezin, G. T., de Quadros, R. W., Gava, F. F., & Petronilho, F. (2024). Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats. Inhalation toxicology, 36(3), 174-188. https://doi.org/10.1080/08958378.2024.2322497

Tenfen, L, Simon Machado, R, Mathias, K, Piacentini, N, Joaquim, L, Bonfante, S, Danielski, LG, Engel, NA, da Silva, MR, Rezin, GT, de Quadros, RW, Gava, FF & Petronilho, F 2024, 'Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats', Inhalation toxicology, vol. 36, no. 3, pp. 174-188. https://doi.org/10.1080/08958378.2024.2322497

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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 = "acute lung injury, Hyperoxia, lung, oxidative stress, oxygen",

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

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year = "2024",

doi = "10.1080/08958378.2024.2322497",

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AU - Simon Machado, Richard

AU - Mathias, Khiany

AU - Piacentini, Natalia

AU - Joaquim, Larissa

AU - Bonfante, Sandra

AU - Danielski, Lucineia Gainski

AU - Engel, Nicole Alessandra

AU - da Silva, Mariella Reinol

AU - Rezin, Gislaine Tezza

AU - de Quadros, Rafaella Willig

AU - Gava, Fernanda Frederico

AU - Petronilho, Fabricia

PY - 2024

Y1 - 2024

N2 - 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.

AB - 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.

KW - acute lung injury

KW - Hyperoxia

KW - lung

KW - oxidative stress

KW - oxygen

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

Abstract

Keywords

ASJC Scopus subject areas

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