Reactive oxygen species: Oxidative damage and pathogenesis

Reactive oxygen species (ROS) such as O-2(-), H2O2 and (OH)-O-. are highly toxic to cells. Cellular antioxidant enzymes, and the free-radical scavenge rs normally protect a cell from toxic effects of the ROS, However, when gen eration of the ROS overtakes the antioxidant defense of the cells, oxidativ e damage of the cellular macromolecules (lipids, proteins, and nucleic acid s) occurs, leading finally to various pathological conditions, ROS-mediated lipid peroxidation, oxidation of proteins, and DNA damage are well-known o utcomes of oxygen-derived free radicals, leading to cellular pathology and ultimately to cell death. The mechanism of ROS-mediated oxidative damage of lipids, proteins, and DNA has been extensively studied. The site-specific oxidative damage of some of the susceptible amino acids of proteins is now regarded as the major cause of metabolic dysfunction during pathogenesis, R OS have also been implicated in the regulation of at least two well-defined transcription factors which play an important role in the expression of va rious genes encoding proteins that are responsible for tissue injury. One o f the significant benefits of the studies on ROS will perhaps be in designi ng of a suitable antioxidant therapy to control the ROS-mediated oxidative damage, and the disease processes.