ABSTRACT
There is a growing body of evidence suggesting that oxidative stress plays a key role in the pathophysiology of neurodegenerative disease (1-6). Reactive oxygen species (ROS), including free radicals, are produced as a result of normal and aberrant cellular reactions (7-10). ROS are known to cause neuronal cell damage by way of three main mechanisms: protein oxidation, DNA oxidation, and lipid peroxidation. The major ROS are superoxide anions, hydroxyl radical, and hydro gen peroxide (10). Antioxidative defense mechanisms exist to protect against the effects of ROS. These include enzyme systems (catalase, glutathione peroxidase, superoxide dismutase, and quinone reductase) and antioxidant vitamins (vitamins A, C, and E). Evidence suggests that these free radical scavenger systems lose efficiency with aging and that this age-associated increase in oxidative stress plays a major role in neurodegenerative processes (11). In addition, these mecha nisms may play a role in neurodegenerative diseases not associated with aging.
