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Various antioxidant pathways encompass the integrated network of biochemical processes designed to neutralize reactive oxygen species (ROS) and maintain cellular redox balance (Source: StatPearls, "Antioxidants"). These pathways include enzymatic defenses such as superoxide dismutase (SOD), catalase, and the glutathione system, as well as the master regulatory Nrf2-Keap1 signaling axis (Source: Nature Reviews Drug Discovery, "The Nrf2–Keap1 pathway of oxidative stress adaptation"). Under physiological conditions, these systems prevent oxidative damage to essential macromolecules like DNA, proteins, and lipids. In many diseases, including neurodegeneration and cardiovascular disorders, these pathways are overwhelmed, leading to chronic oxidative stress (Source: NIH, "Oxidative Stress and Cancer"). Therapeutic strategies often involve the use of small molecules like Dimethyl fumarate to induce these pathways or provide exogenous antioxidant support (Source: PubChem). However, the complexity of these systems means that non-specific modulation can lead to unintended consequences, such as the protection of malignant cells or the disruption of necessary redox-dependent signaling (Source: PubMed, "The Antioxidant Paradox").
Mechanisms include the activation of the Nrf2-ARE signaling pathway to induce phase II detoxification enzymes, direct scavenging of reactive oxygen species (ROS), and replenishment of the endogenous glutathione pool (Source: PMC, "Antioxidant mechanisms of action").
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