Oxidants, Antioxidants and Disease Prevention - Aara-Super food

2 Concise Monograph Series
FIGURE 1. Examples of free radical reactions
Enzymatic free radical formation
Xanthine oxidase
urate + O 2
.
Xanthine + O - + 2H +
2 + H 2 O
NADPH oxidase
NADPH + 2O NADP + + 2O 2
. - + H +
2
NADPH+ 2 quinone
Cytochrome P450
reductase
NADP + + 2 semiquinone . + H +
Nonenzymatic free radical formation
Fe 2 + H 2 O 2 . Fe 3+ + OH + OH -
Fe 2 + O 2 Fe 3+ + O 2
. -
Lipid oxidation by radical attack (L = lipid)
. . LH + OH L + H 2 O
L . + O 2 LOO .
LOO . + LH LOOH + L . Chain reaction
effects on proteins may play a role in the causation of
cataracts, effects on DNA a re involved in cancer
causation, and effects on lipids apparently contribute to
the causation of atherosclerosis.
Free radicals and other reactive oxygen species in the
human body are derived either from normal, essential
metabolic processes or from external sources. Examples
of both are shown in Table 2.
Free radicals are not always harmful. It is important to
note that they also serve useful purposes in the human
body. For example, free radicals play a role in the
destruction of disease-causing microbes by specialised
blood cells called phagocytes.
Defences against oxidants
The human body has several mechanisms for defence
against free radicals and other reactive oxygen species.
The various defences are complementary to one another
because they act on different oxidants or in different
cellular compartments. One important line of defence is
a system of enzymes, including glutathione peroxidases,
superoxide dismutases and catalase, which
d e c rease the concentration of the most harmful
oxidants. Figure 3 shows some of the actions of these
enzymes. Superoxide dismutases are a family of
antioxidant enzymes which are important in the
catalytic decomposition of the superoxide radical to
hydrogen peroxide and oxygen. Catalase specifically