Nonheme food
ferritin (FTN)
iron minerals, nonheme
iron complexes, and
heme iron contribute to the balance between food
iron absorption and body
iron homeostasis.
Iron absorption depends on
membrane transporter proteins DMT1, PCP/HCP1,
ferroportin (FPN), TRF2, and
matriptase 2. Mutations in DMT1 and
matriptase-2 cause
iron deficiency; mutations in FPN, HFE, and TRF2 cause
iron excess. Intracellular
iron homeostasis depends on coordinated regulation of
iron trafficking and storage
proteins encoded in
iron responsive
element (IRE)-
mRNA. The noncoding IRE-
mRNA structures bind
protein repressors, IRP1 or 2, during
iron deficiency. Integration of the IRE-
RNA in translation regulators (near the cap) or turnover elements (after the coding region) increases
iron uptake (DMT1/TRF1) or decreases
iron storage/efflux (FTN/FPN) when IRP binds. An antioxidant response element in FTN
DNA binds Bach1, a
heme-sensitive
transcription factor that coordinates expression among
antioxidant response
proteins like FTN,
thioredoxin reductase, and
quinone reductase. FTN, an
antioxidant because Fe(2+) and O(2) (
reactive oxygen species generators) are consumed to make
iron mineral, is also a nutritional
iron concentrate that is an efficiently absorbed, nonheme source of
iron from whole legumes. FTN
protein cages contain thousands of mineralized
iron atoms and enter cells by receptor-mediated endocytosis, an absorption mechanism distinct from transport of nonheme
iron salts (
ferrous sulfate),
iron chelators (
ferric-EDTA), or
heme. Recognition of 2 nutritional nonheme
iron sources, small and large (FTN), will aid the
solution of
iron deficiency, a major public health problem, and the development of new policies on
iron nutrition.