lipidoxidation

Lipid oxidation is the oxidative degradation of lipids, particularly polyunsaturated fatty acids in cell membranes and stored fats. It begins with reactive oxygen species or metal-catalyzed reactions that generate lipid radicals and lipid hydroperoxides, which can break down into reactive aldehydes and other fragments. This process occurs in biological systems under stress and also in foods, where it contributes to rancidity and quality loss.

The chemical mechanism is commonly described in initiation, propagation, and termination steps. Initiation involves abstraction of a hydrogen atom from a fatty acid to form a lipid radical. In propagation, oxygen adds to the lipid radical to yield a lipid peroxyl radical, which abstracts another hydrogen to produce a lipid hydroperoxide and new radicals, sustaining a chain reaction. Termination occurs when radicals pair up to form non-radical products, a process that can be hindered or slowed by antioxidants. Lipid hydroperoxides can decompose into secondary products such as malondialdehyde and 4-hydroxynonenal, which can modify proteins and DNA.

Biological significance includes membrane damage, altered fluidity, and impaired function stemming from lipid peroxidation. While excessive lipid peroxidation is associated with aging and diseases such as atherosclerosis and neurodegeneration, certain lipid-derived aldehydes also participate in signaling at controlled levels. Ferroptosis is a regulated form of cell death that depends on iron and lipid peroxidation.

Measurement and prevention: assays such as TBARS (malondialdehyde) and peroxide value assess oxidation, while LC-MS can quantify specific lipid peroxides and aldehydes. Antioxidants (vitamin E, vitamin C, carotenoids, polyphenols) and enzymes (glutathione peroxidase, catalase, SOD) mitigate oxidation. In foods, protection includes light and metal exclusion, proper storage, and use of antioxidants like BHT or BHA.