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

IF 2 4区医学 Q4 TOXICOLOGY Inhalation Toxicology Pub Date : 2024-03-01 Epub Date: 2024-03-06 DOI:10.1080/08958378.2024.2322497

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

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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.

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短期高氧诱导大鼠肺线粒体呼吸链复合物功能障碍和氧化应激。

背景：氧气疗法是许多低氧血症患者的替代疗法。然而，这种做法可能是危险的，因为氧气与氧化应激的发展密切相关：雄性 Wistar 大鼠暴露于高氧（吸入氧分数为 40%，FIO2）和高氧（FIO2 = 60%）环境中 120 分钟。采集血液和肺组织样本进行气体、氧化应激和炎症分析：结果：高氧（FIO2 = 60%）增加了 PaCO2 和 PaO2，降低了血液 pH 值，并导致血小板减少和淋巴细胞增多。在肺组织中，中性粒细胞浸润、一氧化氮浓度、羰基蛋白形成以及线粒体呼吸链复合物 I 和 II 的活性均有所增加。FIO2 = 60% 会降低 SOD 活性，并引起一些组织学变化：总之，我们通过实验证明，短期暴露于高 FIO2 可导致肺部氧化应激。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Inhalation Toxicology 医学-毒理学

CiteScore

4.10

自引率

4.80%

发文量

审稿时长

6-12 weeks

期刊介绍： Inhalation Toxicology is a peer-reviewed publication providing a key forum for the latest accomplishments and advancements in concepts, approaches, and procedures presently being used to evaluate the health risk associated with airborne chemicals. The journal publishes original research, reviews, symposia, and workshop topics involving the respiratory system’s functions in health and disease, the pathogenesis and mechanism of injury, the extrapolation of animal data to humans, the effects of inhaled substances on extra-pulmonary systems, as well as reliable and innovative models for predicting human disease.