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
{"title":"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。","authors":"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","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>Male Wistar rats were exposed to hyperoxia with a 40% fraction of inspired oxygen (FIO<sub>2</sub>) and hyperoxia (FIO<sub>2</sub> = 60%) for 120 min. Blood and lung tissue samples were collected for gas, oxidative stress, and inflammatory analyses.</p><p><strong>Results: </strong>Hyperoxia (FIO<sub>2</sub> = 60%) increased PaCO<sub>2</sub> and PaO<sub>2</sub>, 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. FIO<sub>2</sub> = 60% decreased SOD activity and caused several histologic changes.</p><p><strong>Conclusion: </strong>In conclusion, we have experimentally demonstrated that short-term exposure to high FIO<sub>2</sub> can cause oxidative stress in the lung.</p>","PeriodicalId":13561,"journal":{"name":"Inhalation Toxicology","volume":null,"pages":null},"PeriodicalIF":2.0000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats.\",\"authors\":\"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\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>Male Wistar rats were exposed to hyperoxia with a 40% fraction of inspired oxygen (FIO<sub>2</sub>) and hyperoxia (FIO<sub>2</sub> = 60%) for 120 min. Blood and lung tissue samples were collected for gas, oxidative stress, and inflammatory analyses.</p><p><strong>Results: </strong>Hyperoxia (FIO<sub>2</sub> = 60%) increased PaCO<sub>2</sub> and PaO<sub>2</sub>, 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. FIO<sub>2</sub> = 60% decreased SOD activity and caused several histologic changes.</p><p><strong>Conclusion: </strong>In conclusion, we have experimentally demonstrated that short-term exposure to high FIO<sub>2</sub> can cause oxidative stress in the lung.</p>\",\"PeriodicalId\":13561,\"journal\":{\"name\":\"Inhalation Toxicology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2024-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Inhalation Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/08958378.2024.2322497\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/3/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Inhalation Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/08958378.2024.2322497","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/3/6 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"TOXICOLOGY","Score":null,"Total":0}
Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats.
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.
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.
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