Chemical Oxidants Acidify Solitary Complex (SC) Neurons in the Rat

Breathing high levels of oxygen (i.e. hyperoxia) causes hyperventilation and unstable breathing in normal and carotid-deafferented animals (1,2). Prolonged exposure to hyperoxia can disrupt central nervous system (CNS) function and result in a condition termed CNS O2 toxicity, the primary sign of which is convulsion (3,4). The mechanism by which hyperoxia stimulates ventilation and disrupts CNS function is unknown; however, these effects are thought to result from increased production of reactive oxygen species (ROS) during hyperoxia and subsequent oxidation of cellular components vital to normal function (4,5). At moderate levels, ROS, including Superoxide and nitric oxide, as well as their reactive nonradical derivatives (e.g. peroxide, S-nitrosothiols), modulate many physiological processes (4,6), including the hypoxic ventilatory response (7). However, at higher concentrations, ROS can result in oxidative stress that damages cellular components and therefore, are toxic to most cells (4,6). For example, ROS have been implicated in central respiratory control disorders, such as central alveolar hypoventilation syndrome (e.g. sudden infant death syndrome)