Hyperoxia and brain: the link between necessity and injury from a molecular perspective.

Oxygen (O2) supplementation is commonly used to treat hypoxia in patients with respiratory failure. However, indiscriminate use can lead to hyperoxia, a condition detrimental to living tissues, particularly the brain. The brain is sensitive to reactive oxygen species (ROS) and inflammation caused by high concentrations of O2, which can result in brain damage and mitochondrial dysfunction, common features of neurodegenerative disorders. Hyperoxia leads to increased production of ROS, causing oxidative stress, an imbalance between oxidants and antioxidants, which can damage tissues. The brain is particularly vulnerable to oxidative stress due to its lipid composition, high O2 consumption rate, and low levels of antioxidant enzymes. Moreover, hyperoxia can cause vasoconstriction and decreased O2 supply to the brain, posing a challenge to redox balance and neurodegenerative processes. Studies have shown that the severity of hyperoxia-induced brain damage varies with inspired O2 concentration and duration of exposure. Therefore, careful evaluation of the balance between benefits and risks of O2 supplementation, especially in clinical settings, is crucial.

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.

From diabetic hyperglycemia to cerebrovascular Damage: A narrative review.

Diabetes mellitus is a globally significant disease that can lead to systemic complications, particularly vascular damage, including cardiovascular and cerebrovascular diseases of relevance. The physiological changes resulting from the imbalance in blood glucose levels play a crucial role in initiating vascular endothelial damage. Elevated glucose levels can also penetrate the central nervous system, triggering diabetic encephalopathy characterized by oxidative damage to brain components and activation of alternative and neurotoxic pathways. This brain damage increases the risk of ischemic stroke, a leading cause of mortality worldwide and a major cause of disability among surviving patients. The aim of this review is to highlight important pathways related to hyperglycemic damage that extend to the brain and result in vascular dysfunction, ultimately leading to the occurrence of a stroke. Understanding how diabetes mellitus contributes to the development of ischemic stroke and its impact on patient outcomes is crucial for implementing therapeutic strategies that reduce the incidence of diabetes mellitus and its complications, ultimately decreasing morbidity and mortality associated with the disease.