Iron in intestinal mucosal cells or stored in the liver (see below) may be transferred into the blood
for transport to other tissues.
The iron (III) storage form must be reduced to iron (II) in order to
cross the plasma membrane.
In the blood, iron (II) is reoxidized to iron (III) by ferroxidase II.
Iron (III) is carried by the serum protein, transferrin.
Transferrin contains two sites that bind iron (III) tightly.
Normally
about 1/9 of the transferrin molecules have iron bound at both sites
about 4/9 of them have iron bound at one site
and about 4/9 have no iron bound.
This means that transferrin is normally only about 1/3 saturated with
iron (the summary of saturation in the list above indicates that about six
out of every 18 sites are occupied), and there is a substantial unsaturated
plasma iron binding capacity. An unexpected influx of iron can be handled
easily.
The iron binding capacity of serum is of clinical interest. It is
accounted for almost entirely by transferrin.
There are three components to the iron binding capacity of
serum.
Serum iron is the concentration of iron present. Normally it is about
100 micrograms of iron per 100 milliliters of blood.
Total iron binding capacity (TIBC) is the maximum amount of iron
that can be bound. Normally this is about 300 micrograms per 100
milliliters.
The unsaturated iron binding capacity (UIBC) is the difference
between the TIBC and the serum iron. It is normally about 200.
Iron binding capacity is used in the differential diagnosis of
certain diseases.
In conditions associated with increased need for iron (iron deficiency
or late pregnancy) TIBC is increased, but saturation is decreased from the
normal 33%.
In hemochromatosis, TIBC is low, but it is saturated.
Certain other clinical conditions are associated with their own
characteristic patterns of TIBC and percent saturation.
