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General antioxidant pathways encompass the complex network of endogenous enzymatic and non-enzymatic systems dedicated to maintaining cellular redox homeostasis [2, 4]. These pathways protect biological macromolecules from oxidative damage by neutralizing reactive oxygen species (ROS) and reactive nitrogen species (RNS) generated during normal metabolism or environmental stress [6, 16]. Key enzymatic components include superoxide dismutase (SOD), catalase, and the glutathione system, which are largely regulated by the transcription factor Nrf2 [4, 6]. In many chronic diseases, such as neurodegeneration, cardiovascular disorders, and cancer, an imbalance between ROS production and antioxidant capacity leads to pathological oxidative stress [5, 13, 16]. Pharmacological interventions target these pathways through Nrf2 activators, enzyme mimetics, or direct scavengers to restore balance [1, 3, 8]. However, the therapeutic use of antioxidants is complicated by the role of ROS as vital signaling molecules, meaning that excessive suppression can interfere with essential processes like immune response and cell signaling [14, 17].
Direct scavenging of reactive oxygen species [9]; activation of the Nrf2-ARE signaling pathway [6]; mimicking of endogenous antioxidant enzymes such as SOD and GPx [3]; chelation of redox-active metal ions [1]; and inhibition of pro-oxidant enzymes like NADPH oxidase and xanthine oxidase [8, 16].
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