Oxidative stress

The imbalance between reactive oxygen species (free radicals) produced inside cells and the body's antioxidant defenses against them. When the scale tips toward the radicals, proteins, lipids, and DNA take damage.

Edited by M. Callahan · Last reviewed 2026-05-10

How researchers study it

Mitochondria, the cell's energy generators, are major sources of reactive oxygen species as a byproduct of electron transport. Immune cells deliberately produce ROS as a weapon against pathogens. Under normal conditions, antioxidant systems — glutathione, catalase, superoxide dismutase, vitamins C and E, and the Nrf2 transcription program — neutralize this output. Disease, age, environmental toxins, and infection can shift the balance (Sies, Redox Biology, 2015).

Researchers measure oxidative stress indirectly via biomarkers such as malondialdehyde (lipid peroxidation), 8-OHdG (DNA oxidation), oxidized glutathione ratio, and protein carbonyls. In COVID-19, multiple studies have reported elevated oxidative-stress biomarkers in serum during acute infection and in some patients with persistent symptoms (Cecchini & Cecchini, Medical Hypotheses, 2020, PubMed 33713030).

Whether targeted antioxidant intervention improves clinical outcomes is a separate question. Large-scale trials of single antioxidants (vitamin E, beta-carotene) for cardiovascular disease and cancer prevention have been largely disappointing — a finding the field has interpreted as evidence that systemic redox biology is more nuanced than "add more antioxidant" (NIH Office of Dietary Supplements: Vitamin E).

Common misconceptions