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Antioxidant capacity enhancement is a pharmacological or physiological process characterized by the upregulation of the body's endogenous defense mechanisms against oxidative stress. Rather than being a single molecular target like a receptor or enzyme, it represents a therapeutic outcome involving multiple pathways, most notably the Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling cascade. This process leads to increased levels and activity of key enzymes such as Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx), which work together to scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS). By maintaining redox homeostasis, enhancing antioxidant capacity protects cellular components—including DNA, proteins, and lipids—from oxidative damage. This strategy is widely investigated for its potential to treat or prevent conditions driven by chronic oxidative stress, such as neurodegeneration, cardiovascular disorders, and metabolic diseases. Drugs interacting with this process range from natural polyphenols like resveratrol to synthetic clinical agents like dimethyl fumarate, which modulate cellular signaling to boost protective enzymatic responses.
Enhancement of antioxidant capacity is primarily achieved through the activation of the Nuclear factor erythroid 2-related factor 2 (NFE2L2/Nrf2) signaling pathway. Upon activation, Nrf2 translocates to the nucleus and binds to the Antioxidant Response Element (ARE), inducing the transcription of genes for endogenous antioxidant enzymes such as Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx), which neutralize reactive oxygen species (ROS).
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