Final answer:
In the absence of iron, transferrin, the protein responsible for iron transport, circulates with fewer iron ions bound, disrupting normal iron metabolism and potentially leading to iron deficiency anemia.
Step-by-step explanation:
When there is an absence of iron, the blood protein transferrin, which normally binds to and transports iron in the body, is not fully saturated and may be found circulating in the bloodstream with fewer iron molecules bound to it.
In typical iron metabolism, transferrin that is partially saturated with iron circulates in the plasma, allowing for the exchange of iron with interstitial and intracellular compartments, known as the 'labile iron pool'. However, in the absence of iron, this process is disrupted, and transferrin cannot fulfill its primary role in iron transport.
Normally, iron is released from transferrin by reduction to Fe2+ form for immediate use in the synthesis of hemoglobin or storage within ferritin. Ferritin, a large protein, uses oxygen to convert Fe2+ to Fe3+ for storage. When the body needs iron, this Fe3+ is again reduced to Fe2+ for solubility.
In the event of an iron shortage, these processes become less efficient, impacting oxygen transport to tissues and the synthesis of various iron-dependent proteins. This can lead to a condition known as iron deficiency anemia, where there are insufficient red blood cells to carry oxygen throughout the body due to a lack of iron integral to hemoglobin formation within red blood cells.