The antioxidant vitamins C and E
The antioxidant vitamins C and E
The antioxidant vitamins C and E
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oxygen-dependent prolyl hydroxylase enzymes in vitro (11,13), its significance to this<br />
“oxygen sensing” pathway in vivo remains to be determined.<br />
Antioxidant Activity<br />
An <strong>antioxidant</strong> has been defined as “a substance that, when present at low concentrations<br />
compared with those of an oxidizable substrate, significantly delays or prevents<br />
oxidation of that substrate” (14). Several properties make vitamin C an ideal<br />
<strong>antioxidant</strong> in biological systems. First, the low one-electron reduction potentials<br />
of ascorbate <strong>and</strong> the ascorbyl radical enable these compounds to react with <strong>and</strong><br />
reduce virtually all physiologically relevant reactive oxygen species (ROS) <strong>and</strong><br />
reactive nitrogen species (RNS), including superoxide, hydroperoxyl radicals,<br />
aqueous peroxyl radicals, singlet oxygen, ozone, nitrogen dioxide, nitroxide radicals,<br />
<strong>and</strong> hypochlorous acid (15). Hydroxyl radicals also react rapidly, although not<br />
preferentially, with vitamin C; hydroxyl radicals are so reactive that they combine<br />
indiscriminately with any substrate at a diffusion-limited rate. Vitamin C also acts<br />
as a co-<strong>antioxidant</strong> by regenerating α-tocopherol from the α-tocopheroxyl radical.<br />
This may be an important function because in vitro experiments have found that αtocopherol<br />
can act as a prooxidant in the absence of co-<strong>antioxidant</strong>s such as vitamin<br />
C (16). Another property that makes vitamin C an ideal <strong>antioxidant</strong> is the low<br />
reactivity of the ascorbyl radical formed when ascorbate scavenges ROS or RNS.<br />
<strong>The</strong> ascorbyl radical is neither strongly oxidizing nor strongly reducing <strong>and</strong> it<br />
reacts poorly with oxygen. Thus, when a reactive radical interacts with ascorbate, a<br />
much less reactive radical is formed. <strong>The</strong> ascorbyl radical scavenges another radical<br />
or rapidly dismutates to form ascorbate <strong>and</strong> DHA. Alternatively, the ascorbyl<br />
radical <strong>and</strong> DHA can be reduced enzymatically or recycled back to ascorbate (see<br />
above).<br />
Dietary Iron Absorption<br />
<strong>The</strong> ability of ascorbate to maintain metals ions in a reduced state is critical to the<br />
function of the mono- <strong>and</strong> dioxygenases discussed above (7,8). Concomitant consumption<br />
of vitamin C from food or supplements enhances nonheme iron absorption<br />
from a single meal in a dose-dependent manner (17), probably because the reduction<br />
of iron by ascorbate makes it less likely to form insoluble complexes with phytate <strong>and</strong><br />
other lig<strong>and</strong>s (1). Iron deficiency is the most common nutrient deficiency in the world<br />
<strong>and</strong> is associated with a number of adverse health effects (18). Consequently, the<br />
potential for increased vitamin C intake to improve iron nutritional status by increasing<br />
the bioavailability of dietary nonheme iron has received considerable attention.<br />
Despite consistent findings of enhanced iron absorption from a single meal in the<br />
presence of vitamin C, several intervention studies were not able to demonstrate that<br />
increasing vitamin C intake improved iron nutritional status (19,20). More recent<br />
research indicates that the enhancing effect of vitamin C on iron absorption from a<br />
complete diet, rather than a single meal, may be offset partially by dietary inhibitors of<br />
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