Lipid peroxidation

[2] It occurs when free radicals, specifically reactive oxygen species (ROS), interact with lipids within cell membranes, typically polyunsaturated fatty acids (PUFAs) as they have carbon–carbon double bonds.

[4] In the initiation phase, a pro-oxidant hydroxyl radical (OH•) abstracts the hydrogen at the allylic position (–CH2–CH=CH2) or methine bridge (=CH−)[clarification needed] on the stable lipid substrate, typically a polyunsaturated fatty acid (PUFA), to form the lipid radical (L•) and water (H2O).

[10] Reactive aldehydes can also form Michael adducts or Schiff bases with thiol or amine groups in amino acid side chains.

[11] The toxicity of lipid hydroperoxides to animals is best illustrated by the lethal phenotype of glutathione peroxidase 4 (GPX4) knockout mice.

These animals do not survive past embryonic day 8, indicating that the removal of lipid hydroperoxides is essential for mammalian life.

[12] It is unclear whether dietary lipid peroxides are bioavailable and play a role in disease, as a healthy human body has protective mechanisms in place against such hazards.

Simplified pathway for lipid autoxidation: Initiated by hydroxyl radical, which abstracts hydrogen and forms a pentadienyl radical (only one resonance structure shown). This radical adds O 2 to give hydroperoxyl radical (red). In a propagation step, this hydroperoxyl radical abstracts an H + atom from a new diene, generating a new pentadienyl radical and a hydroperoxide (blue).
Free radical mechanisms in tissue injury. Lipid peroxidation induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).