Lipid peroxidation (free radical-induced) (null)

Free radicals in lipid membranes refers to the process by which highly reactive free radicals, mainly reactive oxygen species (ROS), attack and oxidize polyunsaturated fatty acids (PUFAs) within cell membrane phospholipids[6][1][5][3]. This process, termed lipid peroxidation, involves a chain reaction with three phases: initiation (formation of a lipid radical), propagation (generation of lipid peroxyl radicals and lipid hydroperoxides), and termination (formation of nonradical products or chain breaking by antioxidants)[6][3]. Lipid peroxidation disturbs membrane structure and function, decreases fluidity, increases permeability, and generates secondary reactive aldehydes (e.g., malondialdehyde, 4-hydroxynonenal) that can form damaging adducts with proteins and DNA[1][3][5]. Dysregulation of this process underlies the pathology of aging, ferroptosis (iron-dependent cell death), atherosclerosis, neurodegeneration, inflammation, and cancer[7][5][1][3]. While not a single molecular target, lipid peroxidation is a damaging biochemical event and a therapeutic target for antioxidant interventions.

Other names

Lipid peroxidationFree radical-induced lipid damageLipid peroxidation in cell membranes

- Radical scavenging (antioxidants such as vitamin E terminate the lipid peroxidation chain reaction by donating electrons to lipid peroxyl radicals) - Iron chelation reduces Fenton reaction-dependent initiation of peroxidation - Enzymatic termination (glutathione peroxidase converts lipid hydroperoxides to non-radical products)