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The reactive oxygen species (ROS) and oxidative stress system refers to the complex network of molecules and pathways involved in the production, regulation, and neutralization of oxygen-derived free radicals and non-radical oxidants (Sies & Jones, 2020, Nature Reviews Molecular Cell Biology). Under physiological conditions, ROS serve as critical signaling molecules in processes such as cell proliferation and immune defense. However, an imbalance between ROS production and the body's antioxidant defenses leads to oxidative stress, causing damage to lipids, proteins, and DNA (Pizzino et al., 2017, Oxidative Medicine and Cellular Longevity). This system is a major driver in the pathogenesis of chronic conditions, including cardiovascular disease, neurodegeneration, and cancer. Therapeutic strategies often focus on modulating specific components of this system, such as activating the Nrf2-Keap1 pathway to enhance endogenous antioxidant production or using small-molecule scavengers to neutralize excess radicals (He et al., 2020, Signal Transduction and Targeted Therapy). Despite its potential, targeting this system is challenging due to the dual role of ROS in both damage and essential cellular signaling, a phenomenon often referred to as the "antioxidant paradox."
Direct scavenging of free radicals, induction of endogenous antioxidant enzymes via Nrf2 activation, inhibition of ROS-producing enzymes such as NADPH oxidase (NOX), and mitochondrial redox modulation.
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