Lipid peroxidation in mitochondria

Lipid peroxidation in mitochondria refers to the process by which reactive oxygen species (ROS), often generated during mitochondrial respiration or under pathological stress, attack polyunsaturated fatty acids within mitochondrial phospholipids, producing lipid radicals and hydroperoxides[2][5][6]. This chain reaction results in membrane damage, loss of mitochondrial function, and can initiate cell death by apoptotic or ferroptotic pathways[1][3][4][7]. Oxidation of specific mitochondrial lipids such as cardiolipin plays a pivotal role in triggering release of pro-apoptotic factors like cytochrome c[3][6]. Mitochondrial lipid peroxidation is a recognized feature of various diseases, including neurodegenerative, cardiovascular, and inflammatory conditions[6][7]. Several mitochondria-targeted antioxidants (e.g., MitoTEMPO, SkQ1, MitoQ) and protective peptides (such as SS31) have been evaluated for their capacity to prevent or mitigate mitochondrial oxidative injury, but as a process, mitochondrial lipid peroxidation itself is not a single molecular target but rather a consequence of mitochondrial dysfunction and oxidative stress[1][6][7].

Other names

mitochondrial lipid peroxidationmitochondrial LPO

Antioxidant scavenging of lipid peroxides (MitoTEMPO, SkQ1, MitoQ); Protection of mitochondrial membrane lipids (SS31); Inhibition of glutathione synthesis to induce LPO (buthionine sulfoximine); Induction of ferroptosis by promoting lipid peroxidation (erastin)