Reactive oxygen species and redox-active metals (ROS/Metals)

Reactive oxygen species (ROS) and redox-active metals, such as iron and copper, are pivotal mediators of cellular redox homeostasis and oxidative stress (Halliwell & Gutteridge, 2015). ROS, including superoxide and hydrogen peroxide, are natural byproducts of mitochondrial metabolism and enzymatic activities like NADPH oxidase, while redox-active metals facilitate the Fenton reaction to generate highly toxic hydroxyl radicals (Sies et al., 2017; Winterbourn, 1995). Pathological accumulation of these species is a hallmark of neurodegenerative diseases like Alzheimer's and Parkinson's, as well as cardiovascular disorders and metal overload syndromes like hemochromatosis (Jomova & Valko, 2011). Pharmacological strategies target these species through scavengers that neutralize radicals and chelators that sequester labile metals to prevent radical formation (Kalinowski & Richardson, 2005). While effective in reducing oxidative damage, these therapies must be carefully managed to avoid disrupting essential redox signaling and causing mineral deficiencies (Forman et al., 2014).

Other names

Free radicalsOxidantsLabile metal ionsTransition metalsReactive oxygen speciesRedox-active metal ions

Direct neutralization of reactive oxygen species through electron donation (scavenging) and sequestration of transition metal ions to prevent the catalytic formation of hydroxyl radicals via the Fenton reaction (chelation) (Halliwell, 2011; Mobarra et al., 2016).