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Lipid radicals are highly reactive chemical species, generated primarily during oxidative stress when free radicals (e.g., hydroxyl, superoxide) attack the fatty acid chains of phospholipids in the phospholipid bilayer, the fundamental component of all cellular membranes[1][6][7]. This initiates lipid peroxidation, a chain reaction that disrupts membrane structure, compromises barrier function, and propagates additional free radicals. The accumulation of lipid radicals can lead to membrane damage, altered membrane fluidity, and cell death pathways such as ferroptosis and apoptosis. Lipid radicals have a central role in the pathophysiology of diseases characterized by oxidative stress, including atherosclerosis, neurodegeneration, and cancer[3][4]. While not themselves a direct therapeutic target, the formation and propagation of lipid radicals are addressed pharmacologically by antioxidants and iron chelators which prevent or terminate free radical-driven damage to cellular membranes.
Scavenging of lipid radicals to interrupt oxidative chain reactions Inhibition of lipid peroxidation Termination of free radical propagation in membranes
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