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