Reactive oxygen species and lipid radicals in phospholipid membranes (ROS/LR)

Reactive oxygen species (ROS) and lipid radicals in phospholipid membranes are critical mediators of oxidative stress and cellular damage. ROS, such as hydroxyl radicals and superoxide, initiate lipid peroxidation by abstracting hydrogen atoms from polyunsaturated fatty acids within the lipid bilayer, generating highly reactive lipid peroxyl and alkoxyl radicals (Ayala et al., 2014, Oxidative Medicine and Cellular Longevity). This autocatalytic chain reaction compromises the structural integrity, fluidity, and permeability of biological membranes, eventually leading to regulated cell death pathways like ferroptosis (Dixon et al., 2012, Cell). These reactive species are central to the pathogenesis of numerous conditions, including neurodegenerative diseases like Alzheimer's and cardiovascular disorders like atherosclerosis (Gaschler & Stockwell, 2017, Biochem Biophys Res Commun). Therapeutic targeting involves the use of radical-trapping antioxidants (RTAs) and scavengers that intercept these radicals to terminate the peroxidation chain (Conrad & Pratt, 2019, Nature Chemical Biology). Drugs such as edaravone are clinically utilized to scavenge these radicals in the treatment of amyotrophic lateral sclerosis and stroke, while experimental compounds like ferrostatin-1 are being developed to specifically inhibit lipid radical-mediated ferroptotic damage.

Other names

Reactive oxygen speciesLipid radicalsLipid peroxyl radicalsLipid alkoxyl radicalsOxidative stress mediatorsMembrane lipid peroxides

Free radical scavenging and chain-breaking antioxidant activity to neutralize reactive species and terminate lipid peroxidation cycles.