ABSTRACT
INTRODUCTION Oxidative stress is hypothesized to contribute to the pathophysiology of age-related macular degeneration (AMD) as well as numerous other chronic, multifactorial conditions, including heart disease, diabetes, and neurodegenerative disorders (1-3). Although reactive oxygen species (ROS) are by-products of normal metabolic processes (e.g., glycolysis and the Krebs cycle), aging and disease may disturb the balance between ROS generation and clearance, resulting in oxidative damage to macromolecules (4). The retina is particularly susceptible to oxidative stress because of its high oxygen consumption, lipid composition, and focused light exposure (4,5). The retinas of AMD patients undergo increased oxidation, as indicated by the greater prevalence of oxidative modifi cations to proteins and DNA in the Bruch’s membrane, drusen, and retinal pigment epithelium (RPE) of AMD patients versus controls (6).
