Reactive oxygen species-mediated oxidative stress pathway (ROS pathway)

Reactive oxygen species (ROS)-mediated oxidative stress is a cellular phenomenon caused by an imbalance between the production and accumulation of reactive oxygen species and a biological system's ability to detoxify these reactive products[7]. ROS include superoxide anion (O₂•⁻), hydrogen peroxide (H₂O₂), hydroxyl radicals (•OH), and singlet oxygen, which are byproducts of normal aerobic metabolism[1][5]. At low levels, ROS function as signaling molecules in redox biology, regulating physiological processes through reversible oxidation of cysteine residues in proteins[1]. However, elevated ROS levels cause oxidative stress, leading to irreversible damage to cellular macromolecules including lipids, proteins, and DNA[1][7]. The mitochondria are the primary source of intracellular ROS, contributing approximately 90% of cellular ROS, mainly from complexes I and III of the electron transport chain[2]. Other sources include NADPH oxidases, the endoplasmic reticulum, and plasma membrane oxidases[2][3]. Cells maintain antioxidant defense systems including superoxide dismutase (SOD), catalase, and glutathione peroxidase to control ROS levels[7]. The dual nature of ROS means they can serve both beneficial signaling functions and pathological roles depending on their concentration and cellular localization[1].

Other names

Oxidative stress pathwayROS signaling pathwayRedox signaling pathwayReactive oxygen species pathway