Iron is an essential biogenic microelement. In the form of hem, it is contained in haemoglobin, myoglobin or cytochromes;
some compounds contain iron bound to a sulphur atom, e.g. aconitase. Iit is also applied in the immune
system. However, it may also be toxic for the organism, so its metabolism must be very strictly regulated. The
regulation of iron metabolism takes place both at the cellular and systemic levels. At the cellular level, there are involved
transferrin receptors controlling the iron influx into the cell, ferritin, and iron regulation proteins (IRPs) - Iron
Responsive Elements (IREs) to control the formation of proteins involved in iron metabolism. At the systemic level,
the liver and the peptide hepcidin are involved. The effect of hepcidin is reduced iron export from duodenal enterocytes
and macrophages and hence reduced iron transfer by transferrin to erythroblasts.
In iron metabolism, vitamin C – ascorbate, is also significantly used. In addition to its known characteristic of improving
the absorption of non-hemic iron in the intestine, it also regulates iron intake into cells and its metabolism. Ascorbate
modulates iron metabolism by stimulating ferritin synthesis, inhibiting lysosomal ferritin degradation, and
reducing cellular efflux of iron. Ascorbate in the plasma membrane is also responsible for ascorbate-stimulated
iron intake from low-molecular iron-citrate complexes that are significant in plasma in case of iron overload diseases.
Recent evidence also suggests that ascorbate is a new modulator of the classical transferrin-iron absorption
pathway, which provides almost all iron for cellular requirements and erythropoiesis under physiological circumstances.
The ability of ascorbate to regulate transferrin-iron uptake can help explain the metabolic disorder that contributes
to ascorbate deficiency-induced anaemia.