Oxygenradikalskader

Oxygenradikalskader, or oxygen radical damage, denotes cellular injury caused by reactive oxygen species (ROS), including superoxide anion, hydrogen peroxide, and hydroxyl radical. ROS are byproducts of normal metabolism, particularly mitochondrial respiration, and are generated during inflammation, immune responses, and exposure to environmental factors such as ultraviolet light and pollutants. Under normal conditions, antioxidant defenses keep ROS at levels that facilitate signaling without causing harm. When production exceeds defenses, oxidative stress occurs and ROS react with cellular components, causing lipid peroxidation, protein oxidation, and nucleic acid modifications that can lead to mutations and cell death.

Consequences of oxygenradikalskader contribute to aging and are linked to a wide range of diseases, notably cancer, cardiovascular disease, and neurodegenerative disorders. Oxidative damage also participates in inflammatory tissue injury and in tissue responses to toxins or radiation. The body mitigates damage with antioxidant enzymes—superoxide dismutase, catalase, and glutathione peroxidase—and non-enzymatic antioxidants such as glutathione, vitamins C and E. Biomarkers of oxidative damage include 8-oxo-2'-deoxyguanosine for DNA lesions and lipid peroxidation products like malondialdehyde.

Prevention focuses on maintaining redox balance through a healthy lifestyle: a diet rich in fruits and vegetables, avoiding smoking and excessive alcohol, minimizing exposure to environmental toxins, and engaging in regular physical activity. The use of high-dose antioxidant supplements is controversial; many studies show mixed or no clear benefit and in some cases potential harm. Ongoing research explores strategies to modulate redox signaling and enhance endogenous antioxidant defenses.