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Lipid peroxidation, or lipid oxidation, is a complex chemical process that leads to oxidative degradation of lipids, [1] resulting in the formation of peroxide and hydroperoxide derivatives. [2] It occurs when free radicals , specifically reactive oxygen species (ROS), interact with lipids within cell membranes , typically polyunsaturated fatty ...
The termination phase involves the interaction of a radical with an antioxidant molecule, such as α-tocopherol (vitamin E), which inhibits the propagation of chain reactions, thus terminating peroxidation. Another method of termination is the reaction between a lipid radical and a lipid peroxide, or the combination of two lipid peroxide ...
Deuterium-reinforced lipids can be used for protecting living cells by slowing the chain reaction of lipid peroxidation. [1] The lipid bilayer of the cell and organelle membranes contain polyunsaturated fatty acids (PUFA) are key components of cell and organelle membranes. Any process that either increases oxidation of PUFAs or hinders their ...
It has been claimed [by whom?] that the α-tocopherol form is the most important lipid-soluble antioxidant, and that it protects membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction. [92] [95] This removes the free radical intermediates and prevents the propagation reaction from continuing.
The free radical chain reaction is sometimes referred to as the Bolland-Gee mechanism [6] [7] or the basic autoxidation scheme (BAS) [8] and was originally based on the oxidation of rubbers, [9] but remains generally accurate for many materials.
Thiobarbituric acid reactive substances (TBARS) are formed as a byproduct of lipid peroxidation (i.e. as degradation products of fats) which can be detected by the TBARS assay using thiobarbituric acid as a reagent. TBARS can be upregulated, for example, by heart attack [1] or by certain kinds of stroke. [2]
Irwin Fridovich and Joe McCord at Duke University discovered the enzymatic activity of superoxide dismutase in 1968. [5] SODs were previously known as a group of metalloproteins with unknown function; for example, CuZnSOD was known as erythrocuprein (or hemocuprein, or cytocuprein) or as the veterinary anti-inflammatory drug "Orgotein". [6]
Glutathione peroxidase 4 (GPx4) has a high preference for lipid hydroperoxides; it is expressed in nearly every mammalian cell, though at much lower levels. Glutathione peroxidase 2 is an intestinal and extracellular enzyme, while glutathione peroxidase 3 is extracellular, especially abundant in plasma. [ 4 ]