短期高氧导致大鼠肺线粒体呼吸链复合物功能障碍和氧化应激。
Short-term hyperoxia induced mitochondrial respiratory chain complexes dysfunction and oxidative stress in lung of rats.
机构信息
Graduate Program in Health Sciences, Health Sciences Unit, University of South Santa Catarina, Tubarão, Brazil.
Laboratory of Experimental Neurology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Brazil.
出版信息
Inhal Toxicol. 2024 Mar;36(3):174-188. doi: 10.1080/08958378.2024.2322497. Epub 2024 Mar 6.
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 (FIO) and hyperoxia (FIO = 60%) for 120 min. Blood and lung tissue samples were collected for gas, oxidative stress, and inflammatory analyses.
RESULTS
Hyperoxia (FIO = 60%) increased PaCO and PaO, 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 = 60% decreased SOD activity and caused several histologic changes.
CONCLUSION
In conclusion, we have experimentally demonstrated that short-term exposure to high FIO can cause oxidative stress in the lung.
背景
氧气疗法是许多低血氧症患者的一种替代疗法。然而，这种做法可能很危险，因为氧气与氧化应激的发展密切相关。
方法
雄性 Wistar 大鼠暴露于 40%吸入氧分数（FIO）的高氧环境和 60%FIO 的高氧环境中 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（FIO=60%）增加了 PaCO 和 PaO，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 的活性增加。FIO=60%降低了 SOD 活性并导致了几种组织学变化。
结论
总之，我们通过实验证明，短期暴露于高 FIO 可导致肺部氧化应激。
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