The role of oxygen radicals in traumatic injury: clinical implications

Abstract

Lipid peroxidation is believed to be a major cause of posttraumatic cell damage and death. In patients with head and spinal injuries, this process is believed to contribute significantly to the development of permanent neurological dysfunction. Lipid peroxidation can be inhibited by pharmacological agents such as the antioxidants methylprednisolone and tirilazad mesylate. Animal models of head and spinal cord injuries have been used to investigate the physiological bases of the effects of antioxidants. These studies have found that antioxidants are capable of inhibiting posttraumatic events such as edema, metabolic dysfunction, and ischemia, indicating that lipid peroxidation participates in all of these processes. Early treatment appears to be essential for antioxidant-mediated neuroprotection. The multiple levels at which lipid peroxidation causes damage suggest that pharmacological modulation of this process may be beneficial in the treatment of a wide range of neural injuries.