Lipid peroxidation chain reactions in cellular membranes (LPO)

Lipid peroxidation chain reactions in cellular membranes represent a complex biochemical process where free radicals or enzymes attack polyunsaturated fatty acids (PUFAs), leading to a self-propagating cycle of oxidative damage (MDPI, 2024). This process results in the formation of lipid hydroperoxides and reactive secondary products like malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), which disrupt membrane fluidity, permeability, and the function of membrane-bound proteins (NIH, 2014). It is a central driver of ferroptosis, an iron-dependent form of regulated cell death, and is implicated in the progression of numerous conditions, including Alzheimer's disease, atherosclerosis, and non-alcoholic fatty liver disease (Frontiers, 2025; NIH, 2025). Pharmacological intervention typically involves the use of chain-breaking antioxidants, such as alpha-tocopherol (Vitamin E), or agents that sequester catalytic metal ions like iron to prevent the initiation and propagation of the reaction (NIH, 1992; Walsh Medical Media, 2024). Clinical monitoring of this target often relies on the measurement of stable end-products in blood or urine to assess the extent of systemic oxidative stress and the efficacy of antioxidant therapies (Rupa Health, 2024; ResearchGate, 2026). Additionally, emerging therapies focus on modulating the glutathione peroxidase 4 (GPX4) pathway to enhance the cell's endogenous capacity to neutralize lipid peroxides (Columbia University, 2024).

Other names

Membrane lipid peroxidationPolyunsaturated fatty acid peroxidationLipid autoxidationFerroptotic lipid peroxidation

Chain-breaking antioxidant activity, free radical scavenging, and inhibition of lipid radical propagation (NIH, 1992; PatSnap, 2024).