Endogenous antioxidant enzyme systems

The endogenous antioxidant enzyme system comprises a complex network of proteins, including superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx), which collectively maintain cellular redox homeostasis by neutralizing reactive oxygen species (ROS) (Halliwell & Gutteridge, 2015). These enzymes are critically dependent on specific micronutrient cofactors—such as selenium, zinc, copper, manganese, and iron—to function effectively (Prasad, 2014). Dysregulation of this system leads to oxidative stress, a key driver in the pathogenesis of cardiovascular diseases, neurodegeneration, and cancer (Sies, 2017). Therapeutic strategies involving micronutrient supply aim to bolster these innate defenses by ensuring adequate cofactor availability for enzyme synthesis and activity (Rayman, 2012). For instance, selenium is essential for the synthesis of selenocysteine, the active site residue in GPx, while zinc and copper are required for the structural and catalytic integrity of SOD1 (Rayman, 2012; Prasad, 2014). However, this "target" is actually a physiological pathway involving multiple distinct enzymes rather than a single molecular entity. Precise dosing is required to avoid pro-oxidant effects or systemic toxicity associated with heavy metal accumulation, such as selenosis or copper toxicity. Monitoring biomarkers like SOD activity or malondialdehyde levels can help assess the efficacy of these interventions in clinical settings. Overall, supporting these enzyme systems represents a foundational approach in nutritional medicine and preventive pharmacology.

Other names

Antioxidant defense systemEnzymatic antioxidant networkRedox regulatory systemEndogenous antioxidant defense

Provision of essential micronutrient cofactors (e.g., Se, Zn, Cu, Mn) to increase the catalytic activity and stability of endogenous antioxidant enzymes like glutathione peroxidase (GPx) and superoxide dismutase (SOD), thereby facilitating the neutralization of reactive oxygen species (ROS) (Rayman, 2012; Prasad, 2014).