Lipid auto-oxidation

Both combustion and lipid auto-oxidation are initiated via the creation of a carbon radical (abstraction of a hydrogen atom by HO- from a C-H bond). The rate is inversely proportional to the C-H bond energy. The C-H bond energies of aromatic carbons are so large that the reaction of HO- with benzene usually goes via addition. Thus, conjugated systems can stabilize radicals by... 

Free radicals are very important both in food systems and in biological systems. In food, the process of lipid auto-oxidation and development of rancidity involves a free radical chain mechanism proceeding via initiation, propagation, and termination steps. This lipid peroxidation process is responsible for the development of off-flavors and undesirable chemical compounds in food. In vivo, free radical-initiated auto-oxidation of cellular membrane lipids can lead to cellular necrosis and is an... 

With regard to the different classes of substances, in the DHS extracts, hydrocarbons, which are secondary products of lipid auto-oxidation, ranging from //-hexane to 1-methylnaphthalene were identified. Linear long-chain Ci and Cis hydrocarbons were found in the samples obtained using the SDE method. 

Esterbauer et al. (1991) have demonstrated that /3-carotene becomes an effective antioxidant after the depletion of vitamin E. Our studies of LDL isolated from matched rheumatoid serum and synovial fluid demonstrate a depletion of /8-carotene (Section 2.2.2.2). Oncley et al. (1952) stated that the progressive changes in the absorption spectra of LDL were correlated with the autooxidation of constituent fatty acids, the auto-oxidation being the most likely cause of carotenoid degradation. The observation that /3-carotene levels in synovial fluid LDL are lower than those of matched plasma LDL (Section 2.2.2) is interesting in that /3-carotene functions as the most effective antioxidant under conditions of low fOi (Burton and Traber, 1990). As discussed above (Section 2.1.3), the rheumatoid joint is both hypoxic and acidotic. We have also found that the concentration of vitamin E is markedly diminished in synovial fluid from inflamed joints when compared to matched plasma samples (Fairburn etal., 1992). This difference could not be accounted for by the lower concentrations of lipids and lipoproteins within synovial fluid. The low levels of both vitamin E and /3-carotene in rheumatoid synovial fluid are consistent with the consumption of lipid-soluble antioxidants within the arthritic joint due to their role in terminating the process of lipid peroxidation (Fairburn et al., 1992). 

Esterbauer, H., Juergens, G., Quehenberger, O. and Roller, E. (1987). Auto-oxidation of human low density lipoprotein. Loss of polyunsamrated fatty acids and vitamin E and generation of aldehydes. J. Lipid Res. 28, 495-509. 

Vitamin E (tocopherol) possesses antioxidative properties, which means it can protect polyunsaturated fatty acids from auto-oxidation. Deficiency of vitamin E causes increased peroxidation of lipids, which consequently leads to elevated production of prostaglandins. Increased concentration of prostaglandins, in turn, retards... 

Badings, H.T. 1960. Principles of auto-oxidation processes in lipids with special regard to the development of auto-oxidation off-flavor. Neth. Milk Dairy J. 14, 215-242. 

Chan, H.W.S. 1987. The mechanism of auto-oxidation. In Auto-oxidation of Unsaturated Lipids (H.W.C. Chan, ed.), pp. 1-16, Academic Press, London. 

Day, E.A., Lillard, D.A., Montgomery, M.W. 1963. Auto-oxidation of milk lipids. III. Effect of flavor of the additive interactions of carbonyl compounds at sub-threshold concentrations.. / Dairy Sci. 46, 291-294. 

Karel, M. 1980. Lipid oxidation, secondary reactions, and water activity of foods. In Auto-oxidation in Foods and Biological Systems (M. Simic, M. Karel, eds.), pp. 191-206, Plenum Press, New York. 

Porter, N.A. 1986. Mechanisms for auto-oxidation of polyunsaturated lipids. Acta Chem. Res. 19, 262-268. 

Cause of denaturation. Many hypotheses have been proposed to explain the denaturation of muscle proteins (9-17). These hypotheses include 1) the effects of inorganic salts concentrated into the liquid phase of the frozen system 2) water-activity relations 3) reactions with lipids 4) reaction with formaldehyde derived from trimethyl amine (in fish) 5) auto-oxidation ... 

These initial steps are highly exothermic, which accelerates the auto-oxidation cycle to an explosive rate to give CO, CO2, and H2O as the stable products. Within biological matrices the auto-oxidation and peroxidation of lipids and fats from foodstuffs are important examples of oxygen radical chemistry. In general the initiator is HO- (or HOO ) and the auto-oxidation cycle is carried by -O2-. 

Reduced transition-metal complexes are traditionally implicated as the initiators for the auto-oxidation of fats, lipids, and foodstuffs. However, whether this involves direct activation of O2 or of reduced dioxygen (Oi"-, HOO-, and HOOH) is unclear. Reduced metal plus HOOH yields HO- via Fenton chemistry and probably is the pathway for initiation of auto-oxidation in many systems (see Chapter 4). Although there has been an expectation that one or more of the intermediates from the auto-oxidation of reduced transition metals [Eq. (6-8)] can act as the initiator for the auto-oxidation of organic substrates, direct experimental evidence has not been presented. 

Because HOO- in water is a moderately weak acid (pf HA/ -9)/ at pH 1 about 1% of the biogenerated O2 - exists as HOO-. The latter species is an effective initiator for the auto-oxidation of lipids via their allylic carbons (see discussion in Chapter 5), and probably represents the primary hazard of superoxide production in biological matrices. 

Assay of the enzyme activity is complicated by the fact that 7a-hydroxylation of cholesterol also may occur due to auto-oxidation or secondary to lipid preoxidation. In addition it is difficult to equilibrate exogenous cholesterol with endogenous microsomal cholesterol. 

Two mechanisms for the toxicity of 6-OHDA have been proposed. First, auto-oxidation could generate ROS and subsequently oxidize unsaturated fatty acids of lipids or thiol groups of proteins. Second, 6-OHDA uncouples mitochondrial oxidative phosphorylation (Wagner and Trendelenburg, 1971). Whether the neurotoxicity of 6-OHDA can be attributed to the production of ROS or dihydroxyindoles (for a review, see Thoe-nen and Tranzer, 1973) is not yet defined. Degeneration of nigrostriatal neurons after intracerebral injections of 6-OHDA to rats is potentiated by administration of iron (Ben-Shachar and Youdim,... 

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