Iron and Reactive Oxygen Species (Fe/ROS)

Iron and reactive oxygen species (ROS) represent a critical biochemical axis in cellular physiology and pathology, primarily linked through the Fenton and Haber-Weiss reactions. In these processes, labile iron (Fe2+) reacts with hydrogen peroxide to generate highly reactive hydroxyl radicals, leading to oxidative damage of lipids, proteins, and DNA (Winterbourn, 1995, PubMed: 7590395). This synergy is the hallmark of ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation (Dixon et al., 2012, PubMed: 22624693). Therapeutically, this axis is targeted in conditions of iron overload (e.g., thalassemia) using chelators like deferoxamine, and in neurodegenerative or oncological contexts where oxidative stress drives disease progression (Mobarra et al., 2016, PubMed: 27633100). While not a single protein target, the modulation of the iron-ROS relationship is a key strategy for mitigating tissue damage and inducing selective cell death in cancer (Sies et al., 2017, PubMed: 28174487). Analysts should note that 'Iron / reactive oxygen species' is a composite target system rather than a single molecular entity, requiring multi-modal therapeutic approaches.

Other names

Iron-mediated oxidative stressFenton reaction reactantsLabile iron poolIron-ROS axis

Iron chelation to prevent hydroxyl radical formation via the Fenton reaction and ROS scavenging to inhibit lipid peroxidation and oxidative damage.