Machado Richard Simon, Tenfen Leonardo, Joaquim Larissa, Lanzzarin Everton Venicius Rosa, Bernardes Gabriela Costa, Bonfante Sandra Regina, Mathias Khiany, Biehl Erica, Bagio Érick, Stork Solange de Souza, Denicol Tais, de Oliveira Mariana Pacheco, da Silva Mariella Reinol, Danielski Lucinéia Gainski, de Quadros Rafaella Willig, Rezin Gislaine Tezza, Terra Silvia Resende, Balsini Jairo Nunes, Gava Fernanda Frederico, Petronilho Fabricia
Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Graduate Program in Health Sciences, Health Sciences Unit, University of South Santa Catarina, Tubarão, SC, Brazil.
Laboratory of Experimental Neurology, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciuma, SC, Brazil.
Respir Physiol Neurobiol. 2022 Dec;306:103963. doi: 10.1016/j.resp.2022.103963. Epub 2022 Aug 27.
Oxygen (O) therapy is used as a therapeutic protocol to prevent or treat hypoxia. However, a high inspired fraction of O (FIO) promotes hyperoxia, a harmful condition for the central nervous system (CNS). The present study evaluated parameters of oxidative stress and mitochondrial dysfunction in the brain of rats exposed to different FIO. Male Wistar rats were exposed to hyperoxia (FIO 40 % and 60 %) compared to the control group (FIO 21 %) for 2 h. Oxidative stress, neutrophilic infiltration, and mitochondrial respiratory chain enzymes were determined in the hippocampus, striatum, cerebellum, cortex, and prefrontal cortex after O exposure. The animals exposed to hyperoxia showed increased lipid peroxidation, formation of carbonyl proteins, N/N concentration, and neutrophilic infiltration in some brain regions, like hippocampus, striatum, and cerebellum being the most affected. Furthermore, CAT activity and activity of mitochondrial enzyme complexes were also altered after exposure to hyperoxia. Rats exposed to hyperoxia showed increase in oxidative stress parameters and mitochondrial dysfunction in brain structures.
氧（O）疗法被用作预防或治疗缺氧的治疗方案。然而，高吸入氧分数（FIO）会导致高氧血症，这对中枢神经系统（CNS）是一种有害状态。本研究评估了暴露于不同FIO的大鼠大脑中的氧化应激和线粒体功能障碍参数。将雄性Wistar大鼠与对照组（FIO 21%）相比，暴露于高氧环境（FIO 40%和60%）2小时。在氧暴露后，测定海马体、纹状体、小脑、皮质和前额叶皮质中的氧化应激、中性粒细胞浸润和线粒体呼吸链酶。暴露于高氧环境的动物在一些脑区，如受影响最严重的海马体、纹状体和小脑中，脂质过氧化增加、羰基蛋白形成、N/N浓度增加以及中性粒细胞浸润增加。此外，暴露于高氧环境后，CAT活性和线粒体酶复合物的活性也发生了改变。暴露于高氧环境的大鼠在脑结构中表现出氧化应激参数增加和线粒体功能障碍。
