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Reactive oxygen species (ROS) and oxidative pathways encompass a heterogeneous group of oxygen-derived molecules, such as superoxide, hydrogen peroxide, and hydroxyl radicals, along with the enzymatic systems that regulate their flux (PMC, 2025). Under physiological conditions, ROS function as vital second messengers in signal transduction, regulating processes like cell proliferation, differentiation, and the innate immune response (Antioxid. Redox Signal., 2015). However, an imbalance between ROS production and the body's antioxidant defenses leads to oxidative stress, which causes oxidative damage to DNA, proteins, and lipids (Antioxidants, 2025). This pathological state is a central driver in the progression of diverse conditions, including cancer, neurodegenerative disorders, and cardiovascular diseases (PMC, 2022; PMC, 2025). Therapeutic strategies targeting these pathways range from direct antioxidants and Nrf2 activators that bolster cellular defenses to the targeted inhibition of ROS-generating enzymes like NADPH oxidases (MedChemExpress, 2024). Conversely, certain anti-cancer therapies exploit the sensitivity of tumor cells to oxidative stress by inducing excessive ROS to trigger programmed cell death (PMC, 2024). While ROS and oxidative pathways are frequently cited as therapeutic targets, they represent a broad biological process rather than a single molecular entity (PMC, 2022).
Therapeutic modulation of these pathways involves direct scavenging of reactive species, inhibition of enzymatic sources such as NADPH oxidase (NOX) and xanthine oxidase, or activation of the Nrf2-mediated antioxidant response (Antioxidants, 2025; MedChemExpress, 2024). Additionally, pro-oxidant strategies utilize drugs to deliberately increase ROS levels to trigger apoptosis in susceptible cancer cells (PMC, 2024).
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