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  • Title: Initiation of lipid peroxidation in biological systems.
    Author: Kanner J, German JB, Kinsella JE.
    Journal: Crit Rev Food Sci Nutr; 1987; 25(4):317-64. PubMed ID: 3304843.
    Abstract:
    The direct oxidation of PUFA by triplet oxygen is spin forbidden. The data reviewed indicate that lipid peroxidation is initiated by nonenzymatic and enzymatic reactions. One of the first steps in the initiation of lipid peroxidation in animal tissues is by the generation of a superoxide radical (see Figure 16), or its protonated molecule, the perhydroxyl radical. The latter could directly initiate PUFA peroxidation. Hydrogen peroxide which is produced by superoxide dismutation or by direct enzymatic production (amine oxidase, glucose oxidase, etc.) has a very crucial role in the initiation of lipid peroxidation. Hydrogen peroxide reduction by reduced transition metal generates hydroxyl radicals which oxidize every biological molecule. Hydrogen peroxide also activates myoglobin, hemoglobin, and other heme proteins to a compound containing iron at a higher oxidation state, Fe(IV) or Fe(V), which initiates lipid peroxidation even on membranes. Complexed iron could also be activated by O2- or by H2O2 to ferryl iron compound, which is supposed to initiate PUFA peroxidation. The presence of hydrogen peroxide, especially hydroperoxides, activates enzymes such as cyclooxygenase and lipoxygenase. These enzymes produce hydroperoxides and other physiological active compounds known as eicosanoids. Lipid peroxidation could also be initiated by other free radicals. The control of superoxide and perhydroxyl radical is done by SOD (a) (see Figure 16). Hydrogen peroxide is controlled in tissues by glutathione-peroxidase, which also affects the level of hydroperoxides (b). Hydrogen peroxide is decomposed also by catalase (b). Caeruloplasmin in extracellular fluids prevents the formation of free reduced iron ions which could decompose hydrogen peroxide to hydroxyl radical (c). Hydroxyl radical attacks on target lipid molecules could be prevented by hydroxyl radical scavengers, such as mannitol, glucose, and formate (d). Reduced compounds and antioxidants (ascorbic acid, alpha-tocopherol, polyphenols, etc.) (e) prevent initiation of lipid peroxidation by activated heme proteins, ferryl ion, and cyclo- and lipoxygenase. In addition, cyclooxygenase is inhibited by aspirin and nonsteroid drugs, such as indomethacin (f). The classical soybean lipoxygenase inhibitors are antioxidants, such as nordihydroguaiaretic acid (NDGA) and others, and the substrate analog 5,8,11,14 eicosatetraynoic acid (ETYA), which also inhibit cyclooxygenase (g). In food, lipoxygenase is inhibited by blanching. Initiation of lipid peroxidation was derived also by free radicals, such as NO2. or CCl3OO. This process could be controlled by antioxidants (e).(ABSTRACT TRUNCATED AT 400 WORDS)
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