Oxidative Stress

Abstract

Complex structural and functional changes occur within the blood vessel wall with disease. In peripheral blood vessels, increasing evidence suggests that oxidative stress plays a major role in producing many of these changes.1,2 Oxidative stress occurs as the result of an imbalance between generation of reactive oxygen species (ROS) and antioxidant defense mechanisms. Such stress may occur as a result of increased enzymatic or nonenzymatic generation of superoxide anion (the precursor for multiple ROS and reactive nitrogen species [RNS]) or decreased expression or activity of antioxidant enzymes that tightly regulate subcellular levels of ROS (Figure).3 Although our overall understanding of the importance of oxidative stress in the cerebral circulation lags substantially behind work on blood vessels outside of the brain, there has been an emerging focus into this area. This editorial highlights some recent key findings in relation to cerebral vascular oxidative stress. Schematic illustration of some of the major effects of oxidative and nitrosative stress on the vasculature. Superoxide (O2−) is produced from molecular oxygen by a variety of sources. O2− can directly produce injury or can be converted by superoxide dismutase (SOD) to hydrogen peroxide (H2O2). H2O2 is an important signaling molecule but can also produce injury by forming hydroxyl radical (not shown). Superoxide can react with nitric oxide (NO) to form peroxynitrite (ONOO−). This extremely efficient reaction results in a decrease in NO bioavailability and impaired NO-mediated signaling. In addition, ONOO− may produce additional increases in superoxide as a result …