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Relationship between Oxidative Stress and Inflammation in Hyperoxia Hyperoxia by itself can potentially trigger inflammation by sustaining oxidative stress and/or direct oxidative damage to alveolar macrophages (especially through apoptosis) [253], type I and type II alveolar epithelial cells [273], and pulmonary endothelial cells, in addition to inducing apoptosis in type II bronchiolar terminal and alveolar cells [277,316]

These studies in horses show that the present IU values for natural and synthetic vitamin E underestimate the value of natural vitamin E

These anti-inflammatory effects were found to be mediated by the release of H 2 S via sulfane sulfur metabolism [75]

However, more persistent inflammation changes the phenotype of microglia, making them more active and able to phagocytise astrocyte end-feet and reduce BBB permeability [62]