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The reactive oxygen species (ROS) production and redox system is a complex biological network responsible for the generation and regulation of highly reactive oxygen-containing molecules such as superoxide and hydrogen peroxide (Sies & Jones, 2020). It involves a delicate balance between pro-oxidant sources, including the mitochondrial electron transport chain and NADPH oxidases (NOX), and antioxidant defense mechanisms such as superoxide dismutase (SOD), catalase, and the glutathione system (Di Meo et al., 2016). In physiological conditions, ROS act as critical secondary messengers in signal transduction, gene expression, and immune defense. However, chronic dysregulation leading to oxidative stress results in macromolecular damage to DNA, proteins, and lipids, serving as a key driver in the pathogenesis of cancer, neurodegeneration, and cardiovascular diseases (Forman & Zhang, 2021). Therapeutic strategies targeting this system focus on restoring redox homeostasis through the use of direct antioxidants, Nrf2 pathway activators, or specific inhibitors of ROS-producing enzymes (Hayes et al., 2020). Despite the clear link between oxidative stress and disease, clinical success has been limited by the dual nature of ROS, which are necessary for normal cellular functions. Consequently, broad-spectrum antioxidant therapies often fail, leading to a shift toward more specific molecular targets within the redox network, such as isoform-specific NOX inhibitors or mitochondrial-targeted antioxidants (Gorrini et al., 2013; Murphy & Hartley, 2018).
Modulation of redox-sensitive transcription factors (e.g., Nrf2 activation), direct scavenging of reactive species, or inhibition of ROS-generating enzymes such as NADPH oxidase (NOX) and xanthine oxidase (Sies & Jones, 2020; Hayes et al., 2020).
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