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Reactive oxygen and nitrogen species (ROS/RNS) and lipid peroxidation (LPO) intermediates are highly reactive molecules produced during normal cellular metabolism and in response to environmental stressors (Lushchak, 2014). ROS include species such as superoxide and hydrogen peroxide, while RNS include nitric oxide and peroxynitrite, all of which can cause oxidative damage to DNA, proteins, and lipids when produced in excess (Sies et al., 2017). Lipid peroxidation specifically involves the oxidative degradation of polyunsaturated fatty acids, generating toxic secondary intermediates like malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) that can form damaging adducts (Ayala et al., 2014). While these species are essential at low levels for signal transduction and immune defense, their chronic elevation leads to oxidative stress, a central driver in the pathogenesis of neurodegeneration, atherosclerosis, and cancer (Halliwell & Gutteridge, 2015). Therapeutic strategies utilize antioxidants and radical scavengers, such as Edaravone or N-acetylcysteine, to neutralize these species and mitigate tissue damage (Watanabe et al., 2018). However, the clinical application of these agents is complicated by the dual nature of these molecules, as non-selective scavenging can interfere with vital redox-sensitive signaling pathways (Forman & Zhang, 2021).
Direct scavenging of free radicals and neutralization of reactive non-radical species to prevent oxidative damage to cellular components and inhibit the propagation of lipid peroxidation chains.
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