Oxidative Stress
The imbalance between free radicals and antioxidants that damages cellular DNA
Definition
Oxidative stress is the imbalance between the production of reactive oxygen species (ROS) and the endogenous antioxidant capacity (enzymatic and non-enzymatic) to neutralise them. ROS — superoxide, hydrogen peroxide, hydroxyl radical — are continuously generated as a by-product of mitochondrial metabolism and immune activity. At low doses they are physiological signals (hormesis), but their chronic excess damages membrane lipids (lipid peroxidation), proteins (carbonylation), and DNA (8-OHdG), accelerating cellular ageing.
Detailed explanation
The 'free radical theory of ageing' was proposed by Denham Harman in 1956. Although the simplistic version (antioxidants extend lifespan) has been refuted in multiple clinical trials (high-dose antioxidants may even increase mortality), the fundamental role of chronic oxidative stress in cellular ageing remains central.
Clinical oxidative-stress biomarkers: - Urinary 8-OHdG: DNA oxidative damage - MDA (malondialdehyde): lipid peroxidation - Protein carbonyls: protein oxidative damage - Total glutathione (GSH + GSSG) and ratio: intracellular antioxidant capacity - TAS (Total Antioxidant Status): plasma antioxidant capacity
The modern strategy is not to saturate with external antioxidants (which can interfere with physiological ROS signalling of exercise) but to activate the endogenous Nrf2 pathway — the antioxidant 'master switch' that regulates transcription of >200 protective genes including glutathione peroxidase, superoxide dismutase, and catalase. Evidence-backed Nrf2 activators: sulforaphane from broccoli sprouts, curcumin with piperine, moderate exercise, thermal hormesis (sauna, cryotherapy), caloric restriction.
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