Lipid peroxidation and low-density lipoprotein oxidation

Lipid peroxidation is a chemical process where free radicals—primarily reactive oxygen species—attack polyunsaturated fatty acids within biological membranes or circulating lipoproteins such as low-density lipoprotein (LDL). This leads to the formation of lipid hydroperoxides and secondary products like malondialdehyde. When LDL undergoes oxidative modification ("LDL oxidation"), its apolipoprotein B component is altered, which promotes uptake by macrophages via scavenger receptors rather than the native LDL receptor. This process results in foam cell formation—a hallmark event in early atherogenesis—and contributes to endothelial dysfunction and vascular inflammation. Enzymatic sources implicated include myeloperoxidase, NADPH oxidase, xanthine oxidase, mitochondrial ROS production, uncoupled endothelial nitric oxide synthase, and various metal ions such as copper or iron that catalyze radical generation. While antioxidants can inhibit these processes experimentally—and some drugs like probucol have been shown to reduce susceptibility to oxidation—the translation into effective cardiovascular therapies has been inconsistent. Thus "lipid peroxidation/LDL oxidation" describes a pathological biochemical process rather than a discrete molecular target suitable for direct pharmacological intervention; it is not itself an enzyme, receptor, transporter or similar entity but rather an outcome involving multiple molecular players.

Other names

lipid peroxidationLDL oxidationoxidized LDL (oxLDL)modified LDLMox-LDL (myeloperoxidase-oxidized LDL)

Antioxidants inhibit or delay lipid peroxidation by scavenging free radicals or chelating metal ions involved in the initiation and propagation steps. Iron chelators reduce iron-dependent lipid peroxidation and ferroptosis.