Lipids peroxide value

FD. see Field desorption Fermentation, beer, 95 Ferrous oxidation/xylenol orange (FOX) method, lipid peroxide value (PV) basic protocol, 520-522, 526 characteristics of, 515, 526 modified, 527-528 FID. see Flame ionization detection Filtration, starch isolation, 676 Fish muscle, water retention examples, 320-323 (figs.) methods, 315-323... 

Lipid peroxidation value in rat liver was measured as TBA value or chemiluminescence value. TBA values were measured by the method of Ohkawa et al. (1979). Chemiluminescence was measured by a synchronous single photon counting apparatus, a chemiluminescence detector CLD-100 (Tohoku Electronic Co., Ltd.,) in combination with a personal computer (NEC-980 IVX) used for the detection of light emission from the liver homogenate at 40°C for 500 sec. ... 

Iodine liberation is one of the oldest and most commonly used methods for assessing lipid substrate oxidation. In this method, hydroperoxides and peroxides oxidize aqueous iodide to iodine, which is then titrated with standard thiosulfate solution and starch as endpoint indicator. The peroxide value is calculated as milliequivalents of peroxide oxygen per kilogram of sample. 

The mechanism of iron-initiated superoxide-dependent lipid peroxidation has been extensively studied by Aust and his coworkers [15-18]. It was found that superoxide produced by xanthine oxidase initiated lipid peroxidation, but this reaction was not inhibited by hydroxyl radical scavengers and, therefore the formation of hydroxyl radicals was unimportant. Lipid peroxidation depended on the Fe3+/Fe2+ ratio, with 50 50 as the optimal value [19]. Superoxide supposedly stimulated peroxidation both by reducing ferric ions and oxidizing ferrous ions. As superoxide is able to release iron from ferritin, superoxide-promoted lipid peroxidation can probably proceed under in vivo conditions [16,20]. 

The effects of flavonoids on in vitro and in vivo lipid peroxidation have been thoroughly studied [123]. Torel et al. [124] found that the inhibitory effects of flavonoids on autoxidation of linoleic acid increased in the order fustin < catechin < quercetin < rutin = luteolin < kaempferol < morin. Robak and Gryglewski [109] determined /50 values for the inhibition of ascorbate-stimulated lipid peroxidation of boiled rat liver microsomes. All the flavonoids studied were very effective inhibitors of lipid peroxidation in model system, with I50 values changing from 1.4 pmol l-1 for myricetin to 71.9 pmol I 1 for rutin. However, as seen below, these /50 values differed significantly from those determined in other in vitro systems. Terao et al. [125] described the protective effect of epicatechin, epicatechin gallate, and quercetin on lipid peroxidation of phospholipid bilayers. 

Values (p.mol I-1) of Flavonoids and BHT for the Inhibition of NADPH-Dependent- (I) and CCI4-Dependent (II) Microsomal Lipid Peroxidation... 

Quercetin and rutin suppressed photosensitized hemolysis of human erythrocytes with ho values equal to 40 p.mol l-1 and 150 jjlmt>I I 1, respectively [139]. Suppression of photohemolysis was accompanied by inhibition of lipid peroxidation. Morin inhibited oxygen radical-mediated damage induced by superoxide or peroxyl radicals to the human cells in the cardiovascular system, erythrocytes, ventricular myocytes, and saphenous vein endothelial cells [140]. Rutin protected against hemoglobin oxidation inside erythrocytes stimulated by prooxidant primaquine [141],... 

Values (p.mol I-1) for Inhibitory Effects of Metal-Rutin Complexes and Rutin on Cytochrome c Reduction by Xanthine Oxidase (I), Iron-Catalyzed Microsomal Lipid Peroxidation (II), and Lucigenin-Amplified Microsomal CL (III) [167]... 

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. 

Recently, the high inhibitory efficiency of metalloporphyrins has been shown in lipid peroxidation of rat brain homogenates [346]. It was found that manganese and cobalt porphyrins were very effective inhibitors of lipid peroxidation while iron and especially zinc porphyrins had very weak inhibitory activity, if any. For example, /50 values were equal to 21, 29, 212, 946 pmol 1 1 for CoTBAP, MnTBAP, FeTBAP, and ZnTBAP, respectively, where TBAP is 5,10,15,20-tetrakis [4-carboxyphenyl]porphyrin similar values were obtained for other porphyrin derivatives. 

Figure 3. Changes in concentration of O2, NO and Fe during cellular lipid peroxidation and its inhibition by NO. Shown ate the concentrations of NO and Fe at key time points. Peroxidation, as measured by O2 uptake, was initiated with 20 pM Fe. At 1 min after the addition of Fe 0.9 pM NO was introduced. NO was rapidly depleted and is below the limit of detection at about 4 min. At the time of NO depletion, rapid O2 uptake resumes. This reinitiation of O2 consumption is due to Fe that is still present at 7.2 pM or about 36% of its original value. (From Kelley, E.E., Wagner, BA., Buettner, G.R., and Bums, C.P., 1999, Arch. Biochem. Biophys. 370 97-104).

Figure 5. Inhibitory effect of NO on Fe -induced lipid peroxidation. Shown is the decreased generation of an oxidative marker (thiobarbituric acid reactive substances, TBARS) as a result of 0.9 iM NO. HL-60 cells (5 x loVral) were placed in an O2 monitor and at the designated time points, butylated hydroxytoluene was added and samples were quick frozen for determination of TBARS. The values represent the mean and standard error of 3-5 independent determinations. Also shown for comparison is the residual concentration of O2 after exposure to the the same conditions. This shows a decrease in utilization of O2 in the presence of NO. We conclude that NO reduces TBARS, and the percent inhibition is similar to the poeent inhibition of O2 consumption. (Modified from our data in Kelley, E.E., Wagner, B.A., Buettner, G.R., and Bums, C.P., 1999, Arch. Biochem. Biophys. 370 97-104).

Lipid peroxides are also able to react with other components of parenteral nutrition admixtures (trace elements), causing a drop in pH with the subsequent potential for physical-chemical instability [29]. Table 11 shows the peroxide value and the pH drop in a pure lipid emulsion and a lipid-containing AlO admixture stored in EVA bags under different conditions of temperature and light exposure in the presence and absence of trace elements. 

TABLE 11 Peroxide Value and pH Drop in Pure Lipid Emulsion and AIO Admixture Stored in EVA Bags under Different Conditions of Temperature and Light Exposition in Presence and Absence of Trace Elements... 

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