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Reactive oxygen species (ROS) generating and antioxidant enzyme pathways constitute the primary regulatory network for cellular redox homeostasis (Sies et al., 2017). ROS-generating enzymes, such as NADPH oxidases (NOX), xanthine oxidase, and mitochondrial complexes, produce reactive molecules like superoxide and hydrogen peroxide that serve as critical secondary messengers in signal transduction (Lambeth, 2004). To prevent oxidative damage, the antioxidant system employs enzymes including superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) to neutralize excess ROS (Halliwell & Gutteridge, 2015). An imbalance between these pathways leads to oxidative stress, which is implicated in the pathogenesis of cancer, neurodegenerative disorders, and cardiovascular diseases (Forman & Zhang, 2021). Therapeutic strategies target these pathways by either inhibiting ROS production or enhancing antioxidant capacity, though the dual role of ROS in both physiology and pathology complicates drug development (Sies & Jones, 2020).
Modulation of reactive oxygen species levels through the inhibition of pro-oxidant enzymes or the enhancement/mimicry of antioxidant enzyme activity to restore redox balance.
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