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Reactive oxygen and nitrogen species are highly reactive molecules generated as byproducts of normal aerobic metabolism, inflammation, and environmental exposures. They function both as mediators of physiological signaling (e.g., redox-based second messenger processes) and as agents of molecular damage when present at excessive levels (oxidative/nitrosative stress). RONS can modulate the activity of proteins—typically via oxidation of cysteine and methionine residues—as well as cause damage to DNA, lipids, and cellular structures. Their roles in disease are diverse, contributing to the pathogenesis of cancer, cardiovascular, neurodegenerative, immune, and aging-related disorders. Clinically, modulation of RONS by drugs remains challenging due to the balance between physiological necessity and cytotoxicity, as seen in the limited efficacy of generalized antioxidant strategies in major trials.
Scavenging/neutralization of free radicals (by antioxidants); Enzymatic modulation (increasing or inhibiting RONS-generating or degrading enzymes); Modulation of redox signaling pathways (altering post-translational modifications via oxidation/reduction)
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