The non-haem iron in plants is poorly absorbed in humans. This relates partly to the iron being in the insoluble Fe3+ form of the mineral, a form that is used by plants for storage purposes. In addition, the iron in plants is able to bind to the fibre components of the plant tissues and this inhibits the minerals availability for absorption in the small intestine by removing the iron from solution. The iron in flour from wheat and corn for example is poorly absorbed because it may be bound to the fibre component of the tissues. Negative correlations between faecal dry matter and iron availability, as well as an exponential correlation between iron absorption and the amount of bran in the diet supports the idea that dietary fibre is able to inhibit the absorption of iron through binding. Studies using fruits in order to observe effects of fibre on iron binding have not seen inhibitory effects, and this is thought to relate to the presence of ascorbic and citric acid within the fruits that are able to act as inhibitors of iron and fibre binding.
Chelating agents such as vitamin C (ascorbic acid) and citric acid have been shown to increase the availability of iron for absorption from plant foods (here). The iron binding capacity of dietary fibre is composed mainly of neutral detergent fibre, a classification of fibre that includes structural components of plants such as lignin, cellulose and hemicellulose. Researchers have investigated the factors that cause the binding of iron to neutral detergent fibre using in vitro models1. For example in one study the effects of pH and various chelating agents was tested on the binding capacity of iron to corn and wheat fibre. The results showed that the amount of iron bound to fibre increased with increasing iron concentration in a linear fashion. The binding of iron was greater for wheat fibre compared to corn fibre. The binding of iron was low at a low pH, but increased as pH rose to a maximum binding at pH 7. Therefore at the acidic conditions of the stomach, binding of iron might be inhibited by stomach acid.
Amino acids were able to inhibit the binding of iron to fibre. This was especially true for cysteine, but histidine also inhibited binding. The ability of cysteine to act as a reducing agent, which may convert Fe3+ to Fe2+ is a likely reason. This conversion would solubilise the iron and thus prevent its capacity to bind to iron by putting it into solution. As has been shown before ascorbic acid and citric acid were also able to prevent the binding of iron to fibre, also likely because they are strong reducing agents. Phosphate and calcium were also shown to be strong inhibitors of the binding of iron to fibre, perhaps because they competed for binding sites in the fibre. Phytic acid also prevented the binding of iron to fibre, but this may make the iron unavailable for absorption because the phytic acid itself binds strongly to the iron. The chelating agent ethylenediaminetetraacetic acid (EDTA) was also able to prevent the binding of iron to fibre, presumably because it is a strong chelating agent itself.
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