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Reactive oxygen species (ROS), toxic reactive carbonyl species (RCS), free radicals, and redox-active metals represent a heterogeneous group of highly reactive chemical entities that mediate oxidative and carbonyl stress within biological systems [PMID: 28249116]. ROS and free radicals, such as superoxide and hydroxyl radicals, are natural byproducts of mitochondrial metabolism and immune response but can cause extensive damage to DNA, proteins, and lipids when produced in excess [PMID: 22229205]. Toxic carbonyls, often derived from lipid peroxidation or sugar oxidation, further exacerbate cellular damage by forming stable adducts with macromolecules, a process linked to aging and chronic diseases like diabetes [PMID: 24563248]. Redox-active metals like iron and copper catalyze the formation of the highly destructive hydroxyl radical via the Fenton and Haber-Weiss reactions [PMID: 11115402]. Pharmacological intervention typically involves the use of scavengers, antioxidants, or chelating agents to neutralize these species or prevent their formation [PMID: 30509180]. While these entities are critical drivers of pathology in neurodegeneration, cardiovascular disease, and cancer, they also play essential roles in physiological cell signaling, making systemic inhibition a significant therapeutic challenge [PMID: 25236452].
Neutralization of reactive species through electron donation (scavenging), enzymatic degradation, or sequestration of catalytic metal ions (chelation) [PMID: 30509180].
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