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J. Biol. Chem., Vol. 259, Issue 8, 4896-4903, Apr, 1984
WA Muir, U Hopfer and M King
We have studied Fe(III)-citrate and Fe(II)-ascorbate uptake by purified
intestinal brush-border membrane vesicles from normal (iron-replete) and
iron-deficient mice. In iron-replete mice using a final Fe(III)
concentration of 1.43 microM, 25-30 pmol of Fe(III)/mg of protein were
bound to the membranes versus 65-70 pmol in iron-deficient mice. Fe(II)
uptake in normal mice using a final Fe(II) concentration of 1.79 microM was
1600-1800 pmol/mg of protein versus 3600-4000 pmol in iron- deficient mice.
Evidence that Fe(II) was transported into the vesicles by a membrane
carrier-mediated process was obtained by observing saturation kinetics
under conditions of isotope exchange at equilibrium in mice rendered
iron-deficient, but not in iron-replete mice. Eighty per cent of the
transported Fe(II) could be removed by strong chelating agents. The
remainder was exchangeable with Fe(II) in the medium when measured under
equilibrium conditions. We can explain these results by the following
model; iron uptake appears to be a 2-fold process. The first step is the
transport of Fe(II) across the membrane by a carrier- mediated process
which is biologically regulated. The second step is the subsequent binding
of iron on the inside of the membrane. The number of binding sites is also
regulated by the iron status of the mouse. The membrane binding affinity
for Fe(II) appears to be weaker than that for dithiothreitol but stronger
than for ascorbate.
Iron transport across brush-border membranes from normal and iron- deficient mouse upper small intestine
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