Lipidiperoksidia

Lipidiperoksidia, or lipid peroxidation, is the oxidative degradation of lipids, particularly polyunsaturated fatty acids in cell membranes. It is driven by reactive oxygen species and metal ions, leading to free radical chain reactions that damage membranes and generate reactive aldehydes such as malondialdehyde and 4-hydroxynonenal.

Mechanism occurs in three phases: initiation, propagation, and termination. Initiation involves abstraction of a hydrogen atom from a lipid to form a lipid radical. Propagation sees oxygen add to the lipid radical to form a lipid peroxyl radical, which abstracts a hydrogen from another lipid, yielding lipid hydroperoxide and regenerating the lipid radical. Termination ends the chain through radical–radical recombination or reaction with antioxidants.

Consequences include the formation of lipid hydroperoxides that can decompose into reactive aldehydes, which can cross-link proteins and nucleic acids, alter membrane properties, and promote inflammation and cell death. Secondary products such as MDA and 4-HNE serve as biomarkers of lipid peroxidation and can contribute to cytotoxicity.

Biological relevance encompasses normal aging processes and responses to oxidative stress, and lipid peroxidation is associated with various diseases, including atherosclerosis, neurodegenerative disorders, and diabetes complications. It also affects food quality, contributing to rancidity and flavor changes in fats and oils.

Defense and detection: cells deploy antioxidants such as vitamin E, vitamin C, carotenoids, and enzyme systems like glutathione peroxidase and catalase to limit lipid peroxidation. Detection methods include the TBARS assay for malondialdehyde, measurements of F2-isoprostanes, and chromatographic analyses of aldehydic products.