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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 International Coenzyme Q10 Association is a nonprofit association originally based in Ancona, Italy and currently in Seville, Spain.Since its establishment in 1997, it has promoted biochemical and clinical research on the substance Coenzyme Q10 in an attempt to increase the body of knowledge about the preventive and therapeutic health effects of Coenzyme Q10.
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. [82] [85] This removes the free radical intermediates and prevents the propagation reaction from continuing.
4-Hydroxynonenal, or 4-hydroxy-2E-nonenal or 4-hydroxy-2-nonenal or 4-HNE or HNE, (C 9 H 16 O 2), is an α,β-unsaturated hydroxyalkenal that is produced by lipid peroxidation in cells. 4-HNE is the primary α,β-unsaturated hydroxyalkenal formed in this process. It is a colorless oil.
Assay of TBARS measures malondialdehyde (MDA) present in the sample, as well as malondialdehyde generated from lipid hydroperoxides by the hydrolytic conditions of the reaction. [4] MDA is one of several low-molecular-weight end products formed via the decomposition of certain primary and secondary lipid peroxidation products.
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 ...
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]
The hydroxyl radical can damage virtually all types of macromolecules: carbohydrates, nucleic acids , lipids (lipid peroxidation) and amino acids (e.g. conversion of Phe to m-Tyrosine and o-Tyrosine). The hydroxyl radical has a very short in vivo half-life of approximately 10 −9 seconds and a high reactivity. [5]