Box 4.3 The far-reaching effects of lipid peroxidation

The process of lipid peroxidation has such wide ramifications that it is discussed in several chapters of this book. The purpose of this box is to bring together and summarize these diverse effects and underline their importance.

Reactive oxygen species

• Oxygen is essential to life but paradoxically, reactive forms of oxygen or 'ROS', which are produced during normal metabolism, have the potential to cause extensive damage in the body.

• ROS, which include hydroxyl and superoxide radicals and the non-radicals hydrogen peroxide and singlet oxygen, are not always harmful. For example they are involved in the destruction of pathogens by phagocytes.

• In the absence of adequate defence mechanisms (see below), ROS can attack DNA, proteins and lipids in the body; food lipids may also be oxidized.

Initiation, propagation and termination of lipid peroxidation

• Lipid peroxidation begins by ROS attack on the carbon atoms between the double bonds in polyunsaturated fatty acids and the lipid radicals so formed can propagate chain reactions that generate yet more lipid radicals (Section 2.3.4).

• Peroxidation is accelerated by heating and by catalysts such as transition metal ions (e.g. Cu2+, Fe3+) and haem compounds (Section

• Chain reactions are terminated when antioxidant radicals combine with lipid radicals to halt further propagation (Section 2.3.4). Vitamin E is an example of a natural lipid-soluble antioxidant with this function (Section

Links to food palatability

• Lipid radicals undergo degradation to smaller molecular weight compounds that are associated with changes (either desirable or adverse) in flavour, aroma, colour and texture of foods (Fig. 4.11).

• Controlled oxidation is capable of generating compounds associated with very specific flavours or aromas (Fig. 4.10).

• Unchecked peroxidation can reduce food palatability quite severely.

• Some products of lipid peroxidation can be toxic (Section although food normally is rendered inedible long before the concentration of such compounds has reached toxic levels. Long-chain lipid peroxides are not well absorbed, but lower molecular weight compounds are absorbed and potentially harmful (Section

Links to disease

• The membranes of organs and tissues are packed with polyunsaturated fatty acids. Integrated antioxidant systems (see below) are normally adequate to prevent peroxidation and membrane disruption.

• Disruption of cellular structures may cause antioxidant systems to be ineffective.

• Changes to proteins and DNA resulting from lipid radical attack can initiate or exacerbate disease processes, for example oxidation of LDL fatty acids and apolipoprotein-B in atherosclerosis (Section 5.4.1) and DNA changes in cancer (Section 4.4).

Antioxidant defences

• One type of antioxidant defence is through enzymes that destroy radicals (e.g. superoxide dismutase, glutathione peroxidase) or non-radicals (e.g. catalase).

• Another type of defence is through consumption of antioxidant nutrients in the diet. These may act as radical scavengers (e.g. vitamin E, carotenoids, Section 4.2.4). A large number of diverse compounds with antioxidant properties exists in foods. Little is known about their mechanism of action.

• Some dietary minerals are essential for the function of antioxidant enzymes (e.g. the various isoforms of superoxide dismutase use copper and zinc or manganese as cofactors, whereas an isoform of glutathione peroxidase uses selenium).

function. Vitamin E has anti-inflammatory effects, possibly by interacting with the prostaglandin synthetase that produces inflammatory eicosanoids (Section 2.4) and also appears to stimulate the immune response. a-Tocopherol seems to be involved in the regulation of intercellular signalling and cell proliferation through the modulation of protein kinase C activity. Finally, it may have a role in DNA biosynthesis. The details of each of these 'other functions' are still far from clear and this should provide a fascinating area of future research. Vitamin K

Vitamin K is the generic name given to a group of compounds, having in common a naphthoquinone ring system (menadione) with different side chains (Fig. 4.9). Plants synthesize phylloquinone (vitamin Kj) with a phytyl side chain identical to that in chlorophyll. Bacteria synthesize menaquinones (vitamin K2) the side chains of which comprise 4-13 isoprenyl units (Sections 7.5.2 and 7.5.3). Major dietary sources of vitamin K1 are fresh green leafy vegetables, green beans and some seed oils. Cereals are poor sources and, of animal foods, only beef liver is a significant source. Vitamin K2 is found in fermented foods, such as cheeses and yoghurt and in ruminant liver. Bacteria in the human gut synthesize menaquinones, but there is uncertainty

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