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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are highly reactive molecules that serve as essential signaling mediators in various physiological processes, including cell growth, differentiation, and immune responses (Sies et al., 2017, Nature Reviews Molecular Cell Biology). Cellular redox systems, which include antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, as well as non-enzymatic molecules like glutathione, are responsible for maintaining redox homeostasis by neutralizing excess ROS/RNS (Holmgren, 1985, Annual Review of Biochemistry). When the production of these reactive species exceeds the buffering capacity of the redox systems, oxidative and nitrosative stress occurs, leading to damage of proteins, lipids, and DNA (Forman & Zhang, 2021, Nature Reviews Drug Discovery). This imbalance is a hallmark of numerous diseases, including cancer, neurodegenerative disorders like Alzheimer's, and cardiovascular conditions (Di Meo et al., 2016, International Journal of Molecular Sciences). Pharmacological intervention typically involves the use of antioxidants to scavenge reactive species or the activation of the Nrf2-Keap1 pathway to enhance the expression of endogenous antioxidant genes (Zhang et al., 2010, Toxicology and Applied Pharmacology).
Pharmacological modulation of the ROS/RNS and cellular redox systems involves several mechanisms: direct scavenging of reactive species by antioxidant compounds, induction of endogenous antioxidant enzymes through the activation of the Nrf2-Keap1 signaling pathway, and the targeted inhibition of enzymatic sources of ROS, such as NADPH oxidases (NOX) or xanthine oxidase (Forman & Zhang, 2021, Nature Reviews Drug Discovery; Zhang et al., 2010, Toxicology and Applied Pharmacology).
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