Oxidative damage secondary oxidation products

Fig. 16.1 Progression of oxidation in a food system from formation of radicals through primary and secondary lipid oxidation products to protein damage.

Oxidation indices, 656-72 peroxide determination, 762-3 peroxide value, 656, 657-64 colorimetry, 658-61 definition, 657 direct titration, 657 electrochemical methods, 663-4 IR spectrophotometry, 661-3 NIR spectrophotometry, 663 UV-visible spectrophotometry, 658-61 secondary oxidation products, 656, 665-72 tests for stability on storage, 664-5, 672 thermal analysis, 672 Oxidative amperometiy, hydroperoxide determination, 686 Oxidative cleavage alkenes, 1094-5 double bonds, 525-7 Oxidative couphng, hydrogen peroxide determination, 630, 635 Oxidative damage... 

Orlien et al. (2000) suggested that 500 MPa is a critical pressure for treatment of chicken breast muscle. Up to 500 MPa, no rancidity during chilled storage was observed and the product was similar to the untreated one. Pressure treatments at 600 and 700 MPa resulted in less oxidation, but at 800 MPa lipid oxidation enhanced to the same extent as the level induced by thermal treatment. Increased lipid oxidation was probably related to membrane damage. Wiggers et al. (2004) also demonstrated that high-pressure treatment at 400 or 600 MPa led to a substantial increase in secondary lipid oxidation products in cooked breast chicken when compared to the 200 MPa treatment and the control sample. Storage period also had a considerable influence on the formation of secondary lipid oxidation products, especially in the presence of O2 in the packs stored for 8 days. Hexanal, octanal, and nonanal were identified as products of lipid oxidation. 

Central among the toxic responses to oxidative stress is the induction of apop-totic death (Curtin et al, 2002 Fleury et al, 2002 Polster and Fkskum, 2004 Ryter et al, 2007). While it is clear that it can be an initiator as well as a signaling event within the apoptotic process, the specific mechanisms underlying these remain uncertain. Likely, these responses could be related to the damage of cellular components e.g. DNA, lipids, and polysaccharides. One potential pathway by which ethanol-mediated oxidative stress may elicit apoptosis of neurons is associated with the oxidation of polyunsaturated fatty acids within mitochondria (Ramachandran et al, 2001, 2003). Among the variety of oxidation products of these fatty acids are toxic/pro-apoptotic aldehydes, the most potent being 4-hydrox-ynonenal (Esterbauer et al, 1990 Uchida et al., 1993). This compound readily induces apoptotic death of neurons (Lovell and Markesbery, 2006 Dwivedi et al., 2007) and is produced in neurons secondary to ethanol-related oxidative stress (Ramachandran et al, 2001, 2003)... 

Oxygenated acylglycerols. Lipid peroxidation in biological tissues attracts much attention because of its possible contribution to the functional modulation of biomembranes and lipoproteins. It is believed to be involved in free-radical-mediated damage, carcinogenesis and ageing processes. Research requires specific, sensitive and reproducible procedures to quantify the lipid hydroperoxides in each lipid class as primary products and the alcohols and aldehydes as secondary products of the peroxidation reaction. The identification and quantification of lipid oxidation products is therefore of great practical and theoretical interest and MS has assumed a major role in these analyses as a result of the development of mild ionization techniques. 

Different levels of secondary products of oxidized fats and oils are formed depending on the conditions of heating. Kanazawa et al. (1985), for example, have shown that the secondary product fraction of per-oxidized methyl linoleate consisted of approximately 35% polymers, 25% endoperoxide-rich components and 40% low molecule weight compounds. Approximately 2.6% of the total amount of orally administered radioactive secondary oxidation products was found in the rat liver 12-24 h after administration. This deposition of the secondary products coupled with elevation of serum transaminase activities, an increase in hepatic TEARS and slight hepatic hypertrophy suggest that secondary products of methyl linoleate cause oxidative damage. 

Primary and secondary products, and end-products of lipid peroxidation have all been shown to accumulate in senile cataracts (Babizhayev, 1989b Simonelli et al., 1989). Accumulation of these compounds in the lenticular epithelial membranes is a possible cause of damage preceding cataract formation. In senile cataracts there is also extensive oxidation of protein methionine and cysteine in both the membrane and cytosol components (Garner and Spector, 1980), while in aged normal lenses a lesser extent of oxidation was confined to the membrane. The authors therefore suggested that oxidation of membrane components was a precataract state. 

The mechanism of benzene-induced toxicity appears to involve the concerted action of several benzene metabolites. Benzene is metabolized, primarily in the liver, to a variety of hydroxylated and opened-ring products that are transported to the bone marrow, where secondary metabolism occurs. Metabolites may induce toxicity both by covalent binding to cellular macromolecules and by inducing oxidative damage. Metabolites may also inhibit stromal cells, which are necessary to support growth of differentiating and maturing marrow cells. ... 

Nitrogen oxides (NO ) are formed during the combustion at high temperature of fossil fuels and of biomasses and are blamed for the production of acid rain, the formation of ozone in the troposphere and of secondary particulate matter and for causing a reduction in breathing functionality and damage to the cardio-circulatory system in humans. 

Other indices measure a secondary stage of oxidation, such as the anisidine value (ANV), pointing to formation of carbonyl compounds, capable of undergoing condensation reactions with p-anisidine, and the thiobarbituric acid reactive substance (TBARS) pointing to the presence of malondialdehyde (MDA) in particular. In biological systems, TBARS is of widespread use as a measure for the extent of oxidation damage. Another test for stability of oils to oxidation is based on the development of acidity as secondary product, for example, standards using the Rancimat equipment or a similar setup. 

The inflammatory response changes with time and can be divided into phases. The rapid phase occurs within seconds to minutes and consists of vasodilation, increased blood flow, edema, and pain. The acute phase is characterized by induction of inflammatory genes by NF-kB and other transcription factors. During this phase, moderate amounts of inflammatory mediators are produced. The chronic phase occurs over months to years and is marked by dramatically increased production of inflammatory mediators. The secondary chronic phase of inflammation occurs after years of oxidative damage has degraded blood vessels and tissues. Such chronic inflammation appears to play a role in many disease states, such as arteriosclerosis and cancer. 

---