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Peroxynitrite (ONOO-) and related reactive oxygen species (ROS) are highly reactive chemical entities produced during normal cellular metabolism and immune responses. While low levels of these species are essential for physiological signaling and pathogen defense, their excessive accumulation leads to oxidative and nitrosative stress, causing irreversible damage to DNA, proteins, and lipids [Pacher et al., 2007, Physiol Rev]. Peroxynitrite, specifically formed from the reaction of superoxide and nitric oxide, is a potent oxidant linked to the nitration of tyrosine residues, which alters protein function and contributes to cell death [Radi, 2018, PNAS]. These molecules are central to the pathophysiology of numerous conditions, including neurodegenerative diseases like Alzheimer's, cardiovascular diseases such as atherosclerosis, and chronic inflammatory states [Sies, 2017, Nat Rev Mol Cell Biol]. Therapeutic interventions aim to neutralize these species through direct scavenging, catalytic decomposition, or by modulating the enzymatic sources of their production, such as NADPH oxidases. However, a significant challenge in targeting ROS/RNS is the risk of disrupting essential redox-sensitive signaling pathways required for cellular homeostasis.
Direct scavenging of reactive species, catalytic decomposition of peroxynitrite into non-toxic products, and inhibition of enzymatic sources of oxidant production.
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