Introduction

Iron is one of several metals that are essential for normal cellular processes. Its primary role in mammalian biology is to bind oxygen in hemoglobin and myoglobin. It is also involved in the enzymatic transfer of electrons by cytochromes, peroxidases, ribonucleotide reductases and catalases. However, the same properties that make iron useful for these functions can also lead to cellular damage when iron is present in excess. Normally, proteins constrain the activity of iron, but when their iron-binding capacity is exceeded, free iron promotes the formation of reactive oxygen species that attack cellular lipids, proteins and nucleic acids. Thus, iron balance must be carefully maintained to avoid the deleterious effects of iron deficiency and iron overload. All known disorders of iron metabolism can be considered abnormalities of iron balance.

There is no physiological excretion mechanism for iron: iron losses result only from bleeding and exfoliation of skin and mucosal cells. Under normal conditions, iron enters the body exclusively by dietary absorption, and absorption is meticulously regulated to balance the small losses. Iron balance is disrupted when intake and losses are not matched. Iron deficiency occurs when the dietary iron supply is inadequate, when losses are increased (primarily because of bleeding) or when both of these circumstances are present. Iron overload results when iron absorption is inappropriately increased due to genetic defects in iron regulatory proteins, or when repeated blood transfusions create a substantial iron burden.

Our understanding of the molecular processes of iron metabolism has advanced considerably over the last decade, as new techniques in genetics and molecular biology have been applied to problems in this field. Much of what we have learned has come from the study of animals with spontaneous and induced mutations in genes important for the transport and storage of iron. It is widely assumed that information gleaned from experiments in rodents can be directly extrapolated to humans. It is clear that iron metabolism is very similar among mammalian species, validating this approach.

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