Superoxide dismutase and oxidative stress markers (SOD/OSM)

Superoxide dismutase (SOD) is a critical antioxidant enzyme that catalyzes the dismutation of the superoxide radical into molecular oxygen and hydrogen peroxide, serving as a primary defense against oxidative damage [1]. The term oxidative stress markers refers to a broad suite of systemic or serum indicators, such as malondialdehyde (MDA) and glutathione (GSH), used to quantify the balance between reactive oxygen species (ROS) production and antioxidant capacity [2]. While SOD itself can be a therapeutic target for SOD mimetics like avasopasem manganese, the broader category of oxidative stress markers functions primarily as a pharmacodynamic endpoint to monitor the efficacy of drugs in reducing systemic inflammation and tissue damage [3]. Dysregulation of these markers is a hallmark of various pathologies, including cardiovascular diseases, neurodegeneration, and chronic inflammatory conditions, where excessive ROS production overwhelms endogenous defenses [4]. Consequently, this entry describes a physiological state and a set of clinical biomarkers rather than a single discrete molecular target.

Other names

SODAntioxidant enzymesRedox biomarkersReactive oxygen species markersSerum oxidative stress indicators

Drugs typically act by mimicking the enzymatic activity of SOD to neutralize superoxide radicals, inducing the expression of endogenous antioxidant enzymes via the Nrf2 signaling pathway, or providing exogenous reducing equivalents to lower systemic oxidative stress levels [3, 4].