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Peroxynitrite-mediated nitration pathways involve the biochemical reactions of peroxynitrite (ONOO-), a highly reactive oxidant formed by the rapid, diffusion-controlled reaction of nitric oxide and superoxide radicals [2, 11]. The primary consequence of this pathway is the nitration of tyrosine residues in proteins, leading to the formation of 3-nitrotyrosine, which serves as a stable biomarker of nitroxidative stress [4, 9]. This modification can impair the function of critical enzymes, such as manganese superoxide dismutase (MnSOD) and prostacyclin synthase, and disrupt tyrosine kinase-mediated signaling, contributing to the progression of diseases such as Alzheimer's, atherosclerosis, and chronic inflammation [8, 12, 14]. Therapeutic strategies targeting this pathway include the use of peroxynitrite scavengers and decomposition catalysts, such as ebselen and manganese porphyrins, which aim to neutralize the oxidant before it can cause irreversible cellular damage [5, 13]. However, achieving therapeutic efficacy is complicated by the need to maintain beneficial nitric oxide signaling and the potential physiological roles of peroxynitrite in processes like immune defense and synaptic plasticity [13, 18].
Scavenging of peroxynitrite and its derived radicals (hydroxyl, nitrogen dioxide, and carbonate radicals) or catalytic decomposition of peroxynitrite into non-toxic nitrate.
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