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Radical and metal species encompass a broad range of reactive molecules and ions, including reactive oxygen species (ROS), reactive nitrogen species (RNS), and transition metals like iron and copper. In physiological conditions, these species are critical for cellular signaling, immune response, and enzymatic catalysis; however, their dysregulation leads to oxidative and nitrosative stress (Halliwell & Gutteridge, 2015, Oxford University Press). Excess free radicals cause damage to essential biomolecules such as DNA, proteins, and lipids, contributing to the pathogenesis of cancer, cardiovascular diseases, and neurodegenerative disorders like Alzheimer's and Parkinson's (Sies, 2017, Academic Press). Metal ions can further exacerbate this damage by participating in the Fenton and Haber-Weiss reactions, generating highly toxic hydroxyl radicals (Casarett & Doull's Toxicology, 2019). Pharmacological intervention typically involves the use of antioxidants or radical scavengers (e.g., edaravone) to neutralize reactive species, or chelating agents (e.g., deferoxamine, penicillamine) to bind and remove excess metal ions (StatPearls, 2023). These therapeutic strategies aim to restore redox homeostasis and prevent the progression of chronic inflammatory and degenerative conditions.
Neutralization of reactive species through electron donation (scavenging) or sequestration of metal ions through coordinate bonding (chelation) to prevent oxidative damage.
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