investigated were high and the steps
between successive dietary concentrations
were large. On the other hand, chick liver
Mn concentrations remained relatively
constant at dietary Mn levels of 9.1, 25.8
and 59.7 μg g^1 , compared with reduced
concentrations at 2.8 μg Mn g^1 diet
(Weigand et al., 1988b), indicating a home-
ostatic plateau in liver over a small range
of dietary concentrations.
Manganese in other tissues, including
bone and skin, feathers, head and feet,
increased significantly. Endogenous Mn
excretion in chicks increases with increas-
ing dietary intake, indicating that regula-
tion of endogenous excretion plays a role
in Mn metabolism.
Iron
Although Fe metabolism has been studied
extensively, including various indirect
methods of measuring absorption and
status, there has been relatively little work
done on the quantitative dynamics of Fe
(for reviews of Fe metabolism, see
Bothwell, 1995; Beard and Dawson, 1997).
Iron deficiency is of limited practical
importance in farm animals except for
suckling pigs, whereas it is one of the most
common deficiencies in humans. Iron
absorption takes place mainly in the
duodenum and upper jejunum. Haem Fe is
absorbed more readily than non-haem Fe,
the absorption of which is affected by
many factors. Mucosal ferritin appears to
act as an iron sink in enterocytes and plays
a major role in the regulation of Fe absorp-
tion. Absorbed Fe is distributed to tissues
bound predominantly to the plasma trans-
port protein, transferrin. Most body iron is
cycled continuously from plasma to
erythroid marrow to red cells, and from
senescent red cells back to plasma. Most of
the body pool of iron is in the form of
haemoglobin in red cells and represents
85–90% of non-storage Fe. The main
storage form of Fe is ferritin, of which
about 60% is found in the liver and about
40% in muscles and the reticuloendothelial
system. The amount of storage Fe can vary
considerably. Typically, the adult human
male has a body Fe content of 4 g of which
about 25% is in storage (Bothwell, 1995).
The rate of absorption of dietary Fe is
an inverse function of the size of body Fe
stores. However, when Fe stores are
depleted and anaemia is present, a further
increase in efficiency of absorption occurs,
which suggests that iron absorption is
regulated by demands for erythropoiesis in
addition to the level of stores (Bothwell,
1995). It has been well established,
although mostly by indirect procedures,
that Fe homeostasis is determined by
changes in rate of absorption. Fe absorp-
tion can vary considerably. Absorption of
Fe by 126 subjects consuming wheat rolls
with varying levels of Ca varied from 2.4 to
30% as determined by whole-body count-
ing of^59 Fe (Hallberg et al., 1991). The same
subjects given^59 Fe with ascorbic acid
while fasting absorbed 23–45% of the dose.
The body has limited ability to excrete
iron, and endogenous Fe loss is derived
mainly from normal gastrointestinal blood
loss, desquamated cells and bile. Such
losses are small and represent only about
0.025% of body Fe per day in healthy
human males. From this figure, a biological
half-life of Fe in humans of about 7.6 years
can be calculated. Other losses from
menses, pregnancy, wounds and parasite
infestation are significant and reduce the
half-life. Although some correlation of Fe
losses with Fe status has been observed,
the changes in loss are small, and it has
been proposed that the variations in loss
simply reflect variations in the Fe content
of desquamated cells rather than a regula-
tory process (Bothwell, 1995). Early tracer
studies indicated no relationship between
endogenous Fe loss and dietary intake in
rats, indicating the absence of a role for
endogenous excretion in the homeostasis
of iron. More recently, increases in endo-
genous faecal Fe excreted per day (deter-
mined by the isotope dilution method)
were negligible compared with the reduc-
tion in the percentage true absorption of
Fe by young, growing male rats fed a high-
Fe diet (400 μg g^1 ) compared with an
adequate-Fe diet (40 μg g^1 ) (Kreuzer andTrace Element Dynamics 177