Lipids, hydroperoxidation

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] ... 

Mincing, cooking and maturing expose meat products to oxidative stress for a long time so that antioxidants added for lipid protection are slowly destroyed on storage. Onion juice is a powerful antioxidant in meat products, more efficient than garlic juice. Lipid hydroperoxides are reduced to inactive hydroxyl derivatives by reaction with sulphur compounds present in those juices. 

Lipid hydroperoxides are either formed in an autocatalytic process initiated by hydroxyl radicals or they are formed photochemically. Lipid hydroperoxides, known as the primary lipid oxidation products, are tasteless and odourless, but may be cleaved into the so-called secondary lipid oxidation products by heat or by metal ion catalysis. This transformation of hydroperoxides to secondary lipid oxidation products can thus be seen during chill storage of pork (Nielsen et al, 1997). The secondary lipid oxidation products, like hexanal from linoleic acid, are volatile and provide precooked meats, dried milk products and used frying oil with characteristic off-flavours (Shahidi and Pegg, 1994). They may further react with proteins forming fluorescent protein derivatives derived from initially formed Schiff bases (Tappel, 1956). 

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. ... 

Scheme 2.1 The key reactions that occur during lipid peroxidation, in this scheme, X represents the initiating species, which must be a highiy reactive oxidant, in order to abstract a H atom from a poiyunsaturated fatty-acid chain LH, the iipid substrate LO2, the peroxyi radicai L, the alkyl radical LOOH, the lipid hydroperoxide.

In the previous section, we have described some of the mechanisms that may lead to the fijrmation of lipid hydroperoxides or peroxyl radicals in lipids. If the peroxyl radical is formed, then this will lead to propagation if no chain-breaking antioxidants are present (Scheme 2.1). However, in many biological situations chain-breaking antioxidants are present, for example, in LDL, and these will terminate the peroxyl radical and are consumed in the process. This will concomitandy increase the size of the peroxide pool in the membrane or lipoprotein. Such peroxides may be metabolized by the glutathione peroxidases in a cellular environment but are probably more stable in the plasma comjxutment. In the next section, the promotion of lipid peroxidation if the lipid peroxides encounter a transition metal will be considered. 

Interactions between Lipid Hydroperoxides and Transition Metals... 

In this reaction scheme, the steady-state concentration of peroxyl radicals will be a direa function of the concentration of the transition metal and lipid peroxide content of the LDL particle, and will increase as the reaction proceeds. Scheme 2.2 is a diagrammatic representation of the redox interactions between copper, lipid hydroperoxides and lipid in the presence of a chain-breaking antioxidant. For the sake of clarity, the reaction involving the regeneration of the oxidized form of copper (Reaction 2.9) has been omitted. The first step is the independent decomposition of the Upid hydroperoxide to form the peroxyl radical. This may be terminated by reaction with an antioxidant, AH, but the lipid peroxide formed will contribute to the peroxide pool. It is evident from this scheme that the efficacy of a chain-breaking antioxidant in this scheme will be highly dependent on the initial size of the peroxide pool. In the section describing the copper-dependent oxidation of LDL (Section 2.6.1), the implications of this idea will be pursued further. 

Scheme 2.3 The inhibition of iipid peroxidation by antioxidants, in this scheme, AH represents an antioxidant A, the antioxidant-derived radicai LH, the lipid substrate LOj, the peroxyl radical L, the alkyl radical LOOM, the lipid hydroperoxide.

In summary, in our view the principal fectors that contribute to the oxidizability of LDL assessed by the addition of a transition metal such as copper ate (1) the lipid hydroperoxide content of the LDL particle and (2) the a-tocopherol content. Other chain-breaking antioxidants such as ubiquinol and the carotenoids are present only at low concentrations in most individuals, and are unlikely to make a significant contribution. 

Thomas, C.E. and Jackson, R.L. (1991). Lipid hydroperoxide involvement in copper dependent and independent oxidation of low density lipoproteins. J. Pharmacol. Exp. Ther. 256, 1182-1188. 

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. 

The Possible Mechanisms of the Oxidation of LDL in the Production of Lipid Hydroperoxides... 

Esterbauer et cil. (1992) have studied the in vitro effects of copper on LDL oxidation and have shown that there are three distinct stages in this process. In the first part of the reaction, the rate of oxidation is low and this period is often referred to as the lag phase the lag phase is apparently dependent on the endogenous antioxidant content of the LDL, the lipid hydroperoxide content of the LDL particle and the fatty acid composition. In the second or propagation phase of the reaction, the rate of oxidation is much faster and independent of the initial antioxidant status of the LDL molecule. Ultimately, the termination reactions predominate and suppress the peroxidation process. The extensive studies of Esterbauer et al. have demonstrated the relative importance of the endogenous antioxidants within the LDL molecule in protecting it from oxidative modification. 

O Brien, P.J. (1969). Intracellular mechanisms for the decomposition of a lipid hydroperoxide I. Decomposition of a lipid peroxide by metals ions, haem compounds and nucleophils. Can. J. Biochem. 47, 485-492. 

---