Antioxidant profile improvement

Antioxidant profile improvement refers to the therapeutic or physiological objective of enhancing an organism's capacity to neutralize reactive oxygen species (ROS) and reactive nitrogen species (RNS), thereby mitigating oxidative stress. This is not a specific molecular target such as a single receptor or enzyme, but rather a complex physiological outcome involving the coordination of various enzymatic and non-enzymatic defense systems (Frijhoff et al., 2015). Chronic oxidative stress is a fundamental driver in the pathogenesis of numerous conditions, including atherosclerosis, Parkinson's disease, and type 2 diabetes, where an imbalance between ROS production and antioxidant defense leads to damage of lipids, proteins, and DNA (Gupta et al., 2014). Pharmacological strategies to improve this profile often involve the use of direct radical scavengers or the activation of the Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, which upregulates a broad battery of cytoprotective genes. While optimizing antioxidant status is generally associated with health benefits, excessive or poorly targeted intervention can disrupt vital redox signaling pathways, potentially leading to adverse effects or reduced efficacy of certain cancer treatments (Bast & Haenen, 2013).

Other names

Antioxidant enhancementOxidative stress reductionRedox homeostasis optimizationAntioxidant status improvement

Improvement of the antioxidant profile is achieved through the direct scavenging of free radicals, the induction of endogenous antioxidant enzymes (such as Superoxide dismutase, Catalase, and Glutathione peroxidase) via the activation of the Nrf2-Keap1 signaling pathway, or by providing metabolic precursors for the synthesis of endogenous antioxidants like Glutathione (GSH) (Bast & Haenen, 2013; Gupta et al., 2014).