Oxidative stress refers to an imbalance between the production of reactive oxygen species and the body’s antioxidant defenses. Reactive oxygen species include free radicals such as superoxide and hydroxyl radicals, as well as non radical oxidants like hydrogen peroxide. At low to moderate levels they play normal physiological roles in cell signaling, immune defense, and regulation of blood vessels. Problems arise when their production exceeds the capacity of enzymatic and non enzymatic antioxidant systems.

Key antioxidant enzymes include superoxide dismutase, catalase, and glutathione peroxidase, which convert reactive molecules into less harmful products. Non enzymatic antioxidants such as vitamins C and E, glutathione, carotenoids, and polyphenols also help neutralize reactive oxygen species or repair oxidized molecules.

Persistent oxidative stress damages DNA, lipids, and proteins, disrupting cellular structures and signaling pathways. It is implicated in aging and in the development or progression of many chronic conditions, including atherosclerosis, hypertension, diabetes complications, neurodegenerative diseases, chronic kidney disease, and certain cancers. Oxidative stress in mitochondria is particularly important, as it can impair energy metabolism and trigger cell death pathways.

Research also links oxidative stress to lifestyle and environmental factors such as smoking, air pollution, poor diet, obesity, and physical inactivity. Moderate physical exercise can enhance endogenous antioxidant capacity, while severe or unaccustomed exertion can transiently increase oxidative damage.

Current research explores biomarkers that reflect oxidative damage or antioxidant status, aiming to improve risk assessment and monitor therapy. Interventions under study include dietary patterns rich in natural antioxidants, pharmacological antioxidants, and strategies that indirectly reduce oxidative stress by improving metabolic and inflammatory profiles.