Autoxidation Of Unsaturated Lipids Research Articles

Autoxidation of Unsaturated Lipids in Food Emulsion

Unsaturated lipids having various physiological roles are of significance in biochemistry, nutrition, medicine, and food. However, the susceptibility of lipids to oxidation is a major cause of quality deterioration in food emulsions. The reaction mechanism and factors that influence oxidation are appreciably different for emulsified lipids and bulk lipids. This article gives a brief overview of the current knowledge on autoxidation of oil-in-water food emulsions, especially those that contain unsaturated lipids, which are important in the food industry. Autoxidation of unsaturated lipids in oil-in-water emulsion is discussed, and so also their oxidation mechanism, the major factors influencing oxidation, determination measures, research status, and the problems encountered in recent years. Some effective strategies for controlling lipid oxidation in food emulsion have been presented in this review.

Coexpression of Trypsin Inhibitory and Acceleratory Substances during Autoxidation of Methyl Linolenate

During the autoxidation of methyl linolenate, a group of degradation products capable of inhibiting β-trypsin activity were generated along with the accelerating substances, as also noted in a previous study. Chemical modification of the functional groups indicated the carbonyl and hydroxyl groups of the inhibitory degradation products and e-amino group (s) of trypsin to possibly be essential for the inhibition, but hydroperoxide not necessarily involved in inhibitory activity. The inhibitory degradation products inhibited α-chymotrypsin and lysozyme activity and thus may be inhibitors of various enzymes. There is thus the possibility that enzyme inhibitors and accelerators are generated spontaneously during the autoxidation of unsaturated lipids.

Cytotoxicity and genotoxicity of lipid-oxidation products

The autoxidation of unsaturated lipids contained in oils, fats, and food and the endogenous oxidative degradation of membrane lipids by lipid peroxidation result in the formation of a very complex mixture of lipid hydroperoxides, chain-cleavage products, and polymeric material. Experimental animal studies and biochemical investigations lend support to the hypothesis that lipid-oxidation products, ingested with food or produced endogenously, represent a health risk. The oral toxicity of oxidized lipids is unexpectedly low. Chronic uptake of large amounts of such materials increases tumor frequency and incidence of atherosclerosis in animals. 4-Hydroxynonenal, a chain-cleavage product resulting from omega 6 fatty acids, disturbs gap-junction communications in cultured endothelial cells and induces several genotoxic effects in hepatocytes and lymphocytes. Although the concentrations of the aldehyde needed to produce these effects are in the range expected to occur in vivo, their pathological significance is far from clear. Recent findings strongly suggest that in vivo modification of low-density lipoprotein by certain lipid-peroxidation products (eg, 4-hydroxynonenal and malonaldehyde) renders this lipoprotein more atherogenic and causes foam-cell formation. Proteins modified by 4-hydroxynonenal and malonaldehyde were detected by immunological techniques in atherosclerotic lesions.

Role of Oxidative Stress in Development of Complications in Diabetes

N epsilon-(carboxymethyl)lysine, N epsilon-(carboxymethyl)hydroxylysine, and the fluorescent cross-link pentosidine are formed by sequential glycation and oxidation reactions between reducing sugars and proteins. These compounds, termed glycoxidation products, accumulate in tissue collagen with age and at an accelerated rate in diabetes. Although glycoxidation products are present in only trace concentrations, even in diabetic collagen, studies on glycation and oxidation of model proteins in vitro suggest that these products are biomarkers of more extensive underlying glycative and oxidative damage to the protein. Possible sources of oxidative stress and damage to proteins in diabetes include free radicals generated by autoxidation reactions of sugars and sugar adducts to protein and by autoxidation of unsaturated lipids in plasma and membrane proteins. The oxidative stress may be amplified by a continuing cycle of metabolic stress, tissue damage, and cell death, leading to increased free radical production and compromised free radical inhibitory and scavenger systems, which further exacerbate the oxidative stress. Structural characterization of the cross-links and other products accumulating in collagen in diabetes is needed to gain a better understanding of the relationship between oxidative stress and the development of complications in diabetes. Such studies may lead to therapeutic approaches for limiting the damage from glycation and oxidation reactions and for complementing existing therapy for treatment of the complications of diabetes.

Kinetic analysis of free-radical reactions in the low-temperature autoxidation of triglycerides

The kinetics of the low-temperature autoxidation of triglycerides has been investigated by electron spin resonance spectroscopy. After initial radical production, four reaction stages are found in the overall autoxidation of unsaturated lipids: (1) formation of peroxyl radicals by addition of molecular oxygen to the initial carbon radicals, (2) consumption of oxygen in the autoxidation cycle, (3) decay of the lipid peroxyl radical into allylic and pentadienyl radicals, and (4) recombination of the carbon-centered radicals. Peroxyl radical decay in saturated lipids follows second-order kinetics with an apparent activation energy of ca. 50 kJ/mol. The authors find that, for polyunsaturated lipids, even at quite low temperatures (120 K), the autoxidation process occurs readily and must be considered in the storage of biological samples.

Autoxidation of Unsaturated Lipids

Book Review| October 01 1988 Autoxidation of Unsaturated Lipids Autoxidation of Unsaturated Lipids. H. W.-S. CHAN. Academic PressLondon 1987 pp. 293, £39.50 M. I. GURR M. I. GURR Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1988) 16 (5): 906–907. https://doi.org/10.1042/bst0160906a Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation M. I. GURR; Autoxidation of Unsaturated Lipids. Biochem Soc Trans 1 October 1988; 16 (5): 906–907. doi: https://doi.org/10.1042/bst0160906a Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1988 Biochemical Society1988 Article PDF first page preview Close Modal You do not currently have access to this content.

Initiation of lipid peroxidation in biological systems.

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)

Controlled synthesis of monohydroperoxides by α-tocopherol inhibited autoxidation of polyunsaturated lipids

α-Tocopherol influences product formation during the autoxidation of unsaturated lipids and, if present in sufficient quantity (5%; 0.1M), only cis,trans-conjugated diene monohydroperoxides are formed: the formation of trans,trans-isomers and secondary oxidation products (e.g. hydroperoxyepidioxides) is suppressed. At this high concentration α-tocopherol does not exert its recognised antioxidant effect but allows autoxidation to proceed smoothly and quite rapidly to produce good yields of monohydroperoxides. This property, coupled with preparative high performance liquid chromatography, has been utilised to prepare and isolate the isomeric monohydroperoxides of methyl arachidonate and 2-linoleoyl-1,3-dipalmitoylglycerol.

Ceroid in the placenta: With special reference to meconium staining thereof

1. The presence of ceroid, a yellow globular lipoid pigment, in the placenta is reported. Although ceroid has been found in various pathologic conditions in animals and humans, there has been no report of its occurrence in the placenta.2. The nature, characteristics, and a possible mode of formation of ceroid are reviewed. It is thought to be derived from unsaturated lipids through the process of autoxidation, peroxide formation, and polymerization; it probably represents lipofuscin in an early stage of its oxidation.3. Two types of ceroid are found in the placenta: (1) ceroid associated with meconium staining of the placenta and (2) ceroid associated with necrosis.4. The former type of ceroid is present in macrophages and mesenchymal cells of the amniotic membrane and chorioamniotic plate of meconium-stained placentas. It is probably derived from unsaturated lipids either contained in the meconium or formed by the interaction of meconium and vernix caseosa. Unsaturated lipids then imbibe the amniotic membrane, are phagocytized by the mesenchymal cells and macrophages, and are converted into ceroid through autoxidation. The macrophages are derived from mesenchymal cells of the membrane. The possibility that bilirubin is a precursor, although postulated by a few previous workers, is very remote.5. The latter type of ceroid is seen in necrotic debris of tissues and blood and in trophoblastic or decidual cells undergoing fatty degeneration. It is probably formed, in loco, through autoxidation of unsaturated lipids in the debris. Necrotic tissues and red blood cells may play an important role in the formation of ceroid 25, 26.6. Accumulation of unsaturated lipids in the placenta from either exogenous (from meconium) or endogenous (from tissue breakdown) sources may result in the relative lack of biologic antioxidants, which, in turn, favors the formation of ceriod.7. Of 200 placentas examined, 69, or 34.5 per cent, showed meconium staining of the membrane; of the 69 placentas, ceroid was found in macrophages and mesenchymal cells in 23, or 33 per cent.