Reactive Oxygen Species (ROS) in the Pathophysiology of Rheumatoid Arthritis (RA)

Free radicals are highly reactive molecules that unstable and have extremely short-short half-life. They derived from either oxygen (reactive species, ROS) or nitrogen RNS) in mitochondria, plasma membrane endoplasmic reticulum due to oxidative stress damage. ROS/RNS physiologically useful at low concentrations responsible for the activation of redox-sensitive signaling pathways, phagocytosis infected cells removal abnormal aging cells. The endogenous sources ROS electron transport chain, respiratory burst phagocytes oxidation lipids. These react with biomolecules such as DNA, proteins lipids may cause pathophysiological conditions autoimmunity, carcinogenesis, neurodegenerative diseases. role autoimmune response remains complex they been implicated initiation, generation amplification novel epitopes. also appears play a critical rheumatoid arthritis (RA), systemic disease joints known inflammatory (IA). involved initiation various pathways significant pathophysiology RA.