Oxidative Stress
An imbalance between the production of reactive oxygen species (free radicals) and the body's ability to neutralise them, leading to cellular damage. Oxidative stress contributes to ageing, neurodegeneration, and tissue injury. Some research peptides are investigated for antioxidant and anti-oxidative stress properties.
Technical Context
ROS sources: mitochondrial electron transport chain (main physiological source — approximately 1-2% of electrons leak to form superoxide), NADPH oxidase (NOX enzymes — activated in phagocytes for pathogen killing and in other cells for signalling), xanthine oxidase, and exogenous sources (UV radiation, pollution, drugs). Antioxidant defence: enzymatic (superoxide dismutase → H2O2; catalase → H2O + O2; glutathione peroxidase → H2O using glutathione) and non-enzymatic (glutathione, vitamin C, vitamin E, uric acid). Oxidative stress occurs when ROS production exceeds antioxidant capacity → lipid peroxidation (membrane damage), protein oxidation (enzyme inactivation, peptide degradation — Met→Met(O), Trp→oxyindole), and DNA oxidation (8-oxoguanine — mutagenic). Elamipretide reduces mitochondrial ROS by stabilising cardiolipin → optimising electron transport chain complex organisation → reducing electron leak → less superoxide production. This is a targeted approach to the primary intracellular ROS source rather than a systemic antioxidant scavenging strategy.