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Initiation of change Linked to oxidative- Promotion of growth Uncontrolled at DNA level stress-induced mutation of altered cells growth/local invasion

Malignant tumor formation

Seeding of malignant cells to other organs (metastasis)

Normal Fatty streak Atheroma Occlusion -> myocardial formation linked to oxidation infarction or stroke of low-density lipoprotein

Coronary or carotid artery

Lens of the eye

Lens of the eye

Cataract -» loss of vision

Lens opacities linked to oxidation of crystallin proteins of lens

Cataract -» loss of vision

Figure 4 Antioxidants may help prevent the long-term oxidative changes to DNA, lipid, and protein that lead to age-related disease.

Table 2 Types of antioxidants

Physical barriers prevent ROS generation or ROS access to important biological sites; e.g., UV filters, cell membranes Chemical traps or sinks 'absorb' energy and electrons and quench ROS; e.g., carotenoids, anthocyanidins Catalytic systems neutralize or divert ROS, e.g., the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase

Binding and redox inactivation of metal ions prevent generation of ROS by inhibiting the Haber-Weiss reaction; e.g., ferritin, caeruloplasmin, catechins Sacrificial and chain-breaking antioxidants scavenge and destroy ROS; e.g., ascorbic acid (vitamin C), tocopherols (vitamin E), uric acid, glutathione, flavonoids

ROS, reactive oxygen species.

the non-ROS-producing route of ferrous (Fe(n)) to ferric (Fe(rn)) oxidation and for incorporating released iron into ferritin for 'safe' iron storage. Haptoglobin (which binds released hemoglobin), hemopexin (which binds released hem), and albumin (which binds transition-metal ions and localizes or absorbs their oxidative effects) can also be regarded as antioxidants in that they protect against metal-ion-catalyzed redox reactions that may produce ROS. An overview of the major types of antioxidants within the body and their interactions is given in Table 2 and Figure 5.

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