Lipid hydroperoxide formation

Nitric oxide released by macrophages during inflammation reacts with active oxygen to form peroxynitrite. Peroxynitrite nitrates protein and peroxidizes lipids. y-Tocopherol (the principal form of vitamin E in the United States diet) and a-tocopherol (the major form present in the European diet and in supplements), both protect against peroxynitrite-induced lipid oxidation. [13]. Christen et al. reported that lipid hydroperoxide formation in liposomes is inhibited more effectively by y-tocopherol than a-tocopherol by a non-antioxidant mechanism [14]. However, Goss et al. [15] concluded that the presence of a-tocopherol attenuates nitration of both y-tocopherol and tyrosine, showing that nitration of... 

Table 10.4. Relative activity of food proteins in inhibiting lipid hydroperoxide formation in oil-in-water emulsions...

Metals of transient valency, particularly copper and iron, catalyse the lipid oxidation because they decompose lipid hydroperoxides with formation of free radicals [15.8] and [15.9] ... 

The mechanism of NPYR formation has been studied by Coleman (37) and Bharucha et al. ( ). Coleman (37) reported that the requirement for a high temperature, the inhibitory effects of water and antioxidants, and the catalytic effect of a lipid hydroperoxide are consistent with the involvement of a free radical in the formation of NPYR. Similarly, Bharucha et al. (29) suggested that, since both NPYR and NDMA increase substantially towards the end of the frying process, N-nitros-amine formation during frying of bacon occurs essentially, if not entirely, in the fat phase after the bulk of the water is removed and therefore by a radical rather than an ionic mechanism. These authors speculated that, during the frying of... 

It has been established that carotenoid structure has a great influence in its antioxidant activity for example, canthaxanthin and astaxanthin show better antioxidant activities than 3-carotene or zeaxanthin. 3- 3 3-Carotene also showed prooxidant activity in oil-in-water emulsions evaluated by the formation of lipid hydroperoxides, hexanal, or 2-heptenal the activity was reverted with a- and y-tocopherol. Carotenoid antioxidant activity against radicals has been established. In order of decreasing activity, the results are lycopene > 3-cryptoxanthin > lutein = zeaxanthin > a-carotene > echineone > canthaxanthin = astaxanthin. ... 

Extensive studies in vitro from many groups have confirmed that exposure of LDL to a variety of pro-oxidant systems, both cell-free and cell-mediated, results in the formation of lipid hydroperoxides and peroxidation products, fragmentation of apoprotein Bioo, hydrolysis of phospholipids, oxidation of cholesterol and cholesterylesters, formation of oxysterols, preceded by consumption of a-tocopherol and accompanied by consumption of 8-carotene, the minor carotenoids and 7-tocopherol. 

It has been proposed [2] (Figure 24.1) that after binding to cytochrome, the substrates such as epoxides, A-oxides, nitro compounds, and lipid hydroperoxides accept two electrons and are reduced to the compounds RH(H)2. In contrast, the oxidizable substrates react with the oxygenated P-450 complex (RH)Fe2+02 (RH)Fe3+ 02 -. After transfer the second electron substrate RH is hydroxylated to ROH and cytochrome P-450 is oxidized to the starting Fe3+ state, completing the catalytic cycle. It is possible that hydroxylation proceeds through the formation of hydroxyl and carbon radicals [3], but a true role of free radicals at the final stages of hydroxylation is still obscure. 

As mentioned earlier, MPO-hydrogen peroxide-chloride system of phagocytes induces the formation of lipid peroxidation products in LDL but their amount is small [167-169], It was proposed that HOCL can decompose the lipid hydroperoxides formed to yield alkoxyl radicals [170]. It was also suggested that chloramines formed in this process decompose to free radicals, which can initiate lipid peroxidation [171]. 

Cells may show a low level of autofluorescence at 413 nm when irradiated at 324 nm. This fluorescence dramatically increases when d -parinaric acid (159) is incorporated into the cell membrane, either by intercalation or esteriflcation. Exposure to oxidation stress of cells enriched with the 159 fluorescent probe causes diminution of the fluorescence intensity and is directly correlated with formation of lipid hydroperoxides. Addition of antioxidants, such as Vitamin E (21), abates fluorescence diminution. A blanc run of cells enriched with 159 but not subjected to oxidation stress is necessary to follow the degradation of 159 when exposed to UV irradiation. This method was applied to track lipid oxidation during apoptosis and other phenomena, triggered by toxic compounds such as H2O2, f-BuOOH and cumyl hydroperoxide (27)"° 11,424... 

Hydroperoxide formation by the ene reaction path may lead to formation of conjugated double bonds in polyunsaturated fatty acids (see Section V.A) this reaction is concurrent with POV increase. An increase of the CDV, as measured from the absorbance at 233 nm, therefore indicates oxidation of polyunsaturated lipids. A strong correlation exists between CDV predicted from the absorbance in the 1100 to 2200 nm NIR region and CDV determined by the Ti Ia-64 AOCS official method , by UV spectrophotometry at 233 nm. The method was applied to determine CDV for oxidized soybean oil. A secondary absorption maximum of lesser intensity appears in the 260-280 mn range, and is assigned to ketone dienes . 

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