Dados do Trabalho

Título

Hyperoxia by short-term promotes oxidative damage and mitochondrial dysfunction in rat brain

Resumo

Introduction: Oxygen (O2) is an essential molecule for aerobic life, being the basis of several metabolic reactions. Oxygen therapy is used as a therapeutic protocol to prevent or treat hypoxia. However, a high inspired fraction of O2 (FIO2) promotes hyperoxia, a harmful condition for the central nervous system (CNS). Objectives: The present study evaluated parameters of oxidative stress and mitochondrial dysfunction in the brain of rats exposed to different FIO2 for a short period. Method: Male Wistar rats were exposed to hyperoxia (FIO2 40% and 60%) compared to the control group (FIO2 21%) during 2 hours. Oxidative damage in lipids and proteins, the activity of the antioxidant enzyme catalase (CAT), nitrite/nitrate (N/N) concentration, neutrophilic infiltration, and mitochondrial respiratory chain enzymes were determined in the hippocampus, striatum, cerebellum, cortex, and prefrontal cortex after 120 minutes of exposure. Results: 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. Conclusion: rats exposed to FIO2 > 21% by 2 hours showed increase in oxidative stress parameters and mitochondrial dysfunction in brain structures.

Palavras Chave

Hyperoxia; Brain Injuries; Neuroinflammation