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Reactive oxygen species (ROS) are highly reactive molecules derived from oxygen, such as superoxide and hydrogen peroxide, which function as critical signaling molecules in physiological processes including cell proliferation and immune defense (Sies et al., 2017). Under normal conditions, redox-sensitive signaling pathways maintain cellular homeostasis by balancing ROS production with antioxidant defenses. However, an excess of ROS leads to oxidative stress, causing oxidative damage to DNA, proteins, and lipids, which is implicated in the pathogenesis of cancer, neurodegenerative diseases, and cardiovascular disorders (Finkel & Holbrook, 2000). Drugs targeting these pathways often exhibit non-specific antioxidant activity by directly scavenging free radicals or inducing endogenous antioxidant enzymes like superoxide dismutase (Halliwell, 2011). While these agents, such as N-acetylcysteine and Vitamin C, are used to mitigate oxidative damage, their clinical efficacy is often hampered by the disruption of essential ROS-mediated signaling, a phenomenon known as the "antioxidant paradox" (Gomez-Cabrera et al., 2008). Consequently, this "target" represents a broad biological process rather than a specific molecular entity, making precise pharmacological intervention challenging.
Non-specific scavenging of reactive oxygen species and free radicals, and the induction of endogenous antioxidant defense mechanisms to restore redox homeostasis (PubChem, 2024).
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