Oxidative Stress in Hypoxic-Ischemic Brain Injury

Abstract

Hypoxic-ischemic brain injury (stroke) continues to be the third leading cause of death in the USA. Hypoxia in the absence of ischemia, such as that occurs in individuals with sleep apnea, chronic obstructive pulmonary disease, and a number of other conditions, also represents a major and growing health issue. A great deal has been learned about the processes that contribute to short-term damage and long-term dysfunction of the nervous system after hypoxia or ischemia, and the mechanisms that underlie vulnerability of the brain to hypoxic-ischemic injury. Oxidative stress, due to pathological changes in the homeostasis of reactive oxygen species (ROS), reflecting abnormal production and/or impaired clearance of ROS, has been implicated as a key mechanism that contributes to tissue damage and functional deficits in hypoxic-ischemic brain injury. This chapter will briefly review prior literature on the sources and molecular targets of ROS in hypoxia-ischemia, and will focus on newer studies implicating inflammatory signaling and redox dysregulation in hypoxic-ischemic brain injury.