ROS

Reactive oxygen species (ROS) are partially reduced oxygen-derived molecules including superoxide anion (O₂⁻), hydrogen peroxide (H₂O₂), the hydroxyl radical (•OH), and singlet oxygen (¹O₂). They are generated as obligate by-products of mitochondrial oxidative phosphorylation (principally at Complexes I and III), by NADPH oxidases on phagocytes and other cells, by xanthine oxidase, and through enzymatic and non-enzymatic peroxidation reactions. At low physiological concentrations ROS serve as second messengers (redox signalling) regulating inflammation, growth-factor responses, and cellular differentiation; at supraphysiological concentrations they oxidise lipids, proteins, and DNA, driving cellular damage and accelerating ageing. The endogenous anti-oxidant defence comprises enzymatic systems (superoxide dismutases SOD1/2/3, catalase, glutathione peroxidases) and small-molecule scavengers (glutathione, vitamin C, vitamin E, ubiquinone). Sustained oxidative stress — the imbalance between ROS production and anti-oxidant defence — is a recognised contributor to chronic inflammatory disease, atherosclerosis, neurodegeneration, diabetes complications, and the cellular ageing phenotype. In peptide research, ROS modulation is central to GHK-Cu's mechanistic profile (SOD activation, broad anti-oxidant gene-network upregulation) and to mitochondrial peptide research (SS-31 reduces mitochondrial ROS leak by stabilising cristae structure; Humanin and MOTS-c modulate mitochondrial redox homeostasis).