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Free radicals and lipid peroxides represent a broad category of reactive chemical species that play dual roles as signaling molecules and mediators of cellular damage (Lobo et al., 2010; PMID: 22228951). Free radicals, such as superoxide and hydroxyl radicals, contain unpaired electrons that make them highly reactive toward biological macromolecules like DNA and proteins. Lipid peroxides are specific products of the oxidative degradation of polyunsaturated fatty acids in cell membranes; their accumulation is a hallmark of oxidative stress and serves as the primary driver of ferroptosis, a form of iron-dependent regulated cell death (Ayala et al., 2014; PMID: 24991264; Stockwell et al., 2017; PMID: 29053968). In physiological conditions, controlled levels of reactive species are involved in intracellular signaling pathways, but their overproduction leads to pathological states (Pizzino et al., 2017; PMID: 28819445). These species are implicated in the progression of diverse diseases, including neurodegenerative disorders (e.g., ALS), atherosclerosis, and chronic inflammation. Pharmacological interventions typically focus on neutralizing these species using antioxidant scavengers, such as Edaravone or N-acetylcysteine, or preventing their formation by modulating enzymatic pathways or chelating pro-oxidant metal ions.
Direct neutralization of reactive species through radical scavenging, electron donation, or enzymatic reduction to stable, non-toxic metabolites
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