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Reactive oxygen species (ROS) and transition metal ions, primarily iron and copper, are chemical entities that collectively modulate the cellular redox environment and drive oxidative stress. ROS are oxygen-derived molecules, such as superoxide and hydrogen peroxide, that are produced as natural byproducts of oxygen metabolism and function as secondary messengers in signal transduction (Sies et al., 2017, Nature Reviews Molecular Cell Biology). Transition metal ions act as potent catalysts that facilitate the Fenton and Haber-Weiss reactions, converting relatively stable ROS into the highly toxic hydroxyl radical, which causes irreversible damage to lipids, proteins, and DNA (Halliwell & Gutteridge, 2015, Free Radicals in Biology and Medicine). This synergistic interaction is a central mechanism in the pathogenesis of neurodegenerative diseases like Alzheimer's and Parkinson's, and it is the defining driver of ferroptosis, a form of regulated cell death (Dixon et al., 2012, Cell). Therapeutic strategies targeting these species involve the use of chelating agents to sequester metal ions and antioxidants to scavenge ROS, thereby preventing oxidative damage and preserving cellular integrity.
Chelation of transition metal ions to prevent the catalytic formation of hydroxyl radicals and direct scavenging of reactive oxygen species to mitigate oxidative damage to cellular components.
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