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Antioxidant metabolism is a comprehensive biological process rather than a single molecular target, encompassing the integrated network of enzymes and molecules dedicated to maintaining cellular redox homeostasis. It involves enzymatic scavengers such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, alongside non-enzymatic antioxidants like glutathione and various vitamins (Halliwell & Gutteridge, 2015, Oxford University Press). This system is critical for protecting cellular components—including DNA, proteins, and lipids—from damage caused by reactive oxygen species (ROS) generated during normal mitochondrial respiration or environmental stress (Forman & Zhang, 2021, Free Radical Biology and Medicine). In many diseases, such as cancer and neurodegeneration, the balance of antioxidant metabolism is disrupted, leading to chronic oxidative stress that drives disease progression. Therapeutic interventions often target specific nodes within this pathway, such as the Nrf2 transcription factor, to upregulate the cell's natural defenses (He et al., 2020, Signal Transduction and Targeted Therapy). However, because ROS also serve as essential signaling molecules for cell growth and immune response, broad or excessive modulation of antioxidant metabolism can lead to unintended side effects, sometimes referred to as the antioxidant paradox. Consequently, while it is a major focus of drug development, 'Antioxidant metabolism' represents a broad physiological category rather than a discrete therapeutic receptor or enzyme.
Modulation of antioxidant metabolism typically involves the induction of endogenous antioxidant enzymes through the activation of the Nrf2/ARE signaling pathway, direct chemical scavenging of reactive oxygen species (ROS), or the replenishment of essential thiol-containing molecules like glutathione to restore cellular redox balance (Sies et al., 2017, Nature Reviews Molecular Cell Biology).
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