NADPH oxidase mediates hypersomnolence and brain oxidative injury in a murine model of sleep apnea.

ABSTRACT:

Rationale

Persons with obstructive sleep apnea may have significant residual hypersomnolence, despite therapy. Long-term hypoxia/reoxygenation events in adult mice, simulating oxygenation patterns of moderate-severe sleep apnea, result in lasting hypersomnolence, oxidative injury, and proinflammatory responses in wake-active brain regions. We hypothesized that long-term intermittent hypoxia activates brain NADPH oxidase and that this enzyme serves as a critical source of superoxide in the oxidation injury and in hypersomnolence.

Objectives

We sought to determine whether long-term hypoxia/reoxygenation events in mice result in NADPH oxidase activation and whether NADPH oxidase is essential for the proinflammatory response and hypersomnolence.

Methods

NADPH oxidase gene

SUBMITTER: Zhan G 

PROVIDER: S-EPMC2718406 | biostudies-literature | 2005 Oct

REPOSITORIES: biostudies-literature