Question

In the intestinal absorption of iron, A. the presence of a reductant like ascorbate enhances the availability of iron. B. the regulation of uptake occurs between the lumen and the mucosal cells. C. the amount of apoferritin synthesized in the mucosal cell is directly related to the need for iron by the host. D. iron bound tightly to a ligand, such as phytate, is more readily absorbed than free iron. E. low pH in the stomach inhibits absorption by favoring \(\mathrm{Fe}^{+2}\).

Short answer

Select all that apply. a) Reductants like ascorbate enhance iron availability by converting ferric iron to ferrous iron. b) The regulation of iron uptake occurs at the level of the intestinal mucosal cells. c) The synthesis of apoferritin in mucosal cells is directly related to the need for iron by the host. d) Iron bound tightly to a ligand, such as phytate, promotes its absorption. e) Low pH in the stomach inhibits iron absorption. Answer: a, b, c

Step-by-step solution

Background on Iron Absorption

Iron is an essential element for human health, and its uptake and absorption within the body are tightly regulated processes. In the intestine, iron is absorbed by intestinal mucosal cells, which are responsible for keeping iron levels balanced. Among the factors that influence iron absorption are the presence of reductants, the regulation of uptake by different cell types, binding to ligands, and acidity in the stomach.

Option A: Reductants and Iron Availability

Ascorbate, also known as vitamin C, is a reductant that can help enhance the availability of iron. Reductants like ascorbate convert ferric iron (\(\mathrm{Fe}^{+3}\)) to ferrous iron (\(\mathrm{Fe}^{+2}\)), the latter being more readily absorbed in the intestine. Therefore, this statement is true.

Option B: Regulation of Iron Uptake

The regulation of iron uptake indeed occurs at the level of the intestinal mucosal cells. These cells serve as a barrier between the lumen (the interior of the intestine) and the body. They are responsible for absorbing iron from the luminal contents and transferring it into the bloodstream. Thus, this statement is also true.

Option C: Apoferritin Synthesis and Iron Needs

Apoferritin is a protein that binds to iron in cells and helps to store and transport it within the body. The synthesis of apoferritin in mucosal cells is indeed directly related to the need for iron by the host. This statement is accurate as well.

Option D: Iron Ligand Binding and Absorption

Iron bound tightly to a ligand, such as phytate, is less readily absorbed than free iron. This is because ligands like phytate can form complexes with iron and inhibit its absorption. This statement is not true, making it the incorrect answer.

Option E: Low pH in the Stomach and Iron Absorption

Low pH in the stomach favors conversion of \(\mathrm{Fe}^{+3}\) to \(\mathrm{Fe}^{+2}\). As stated earlier, ferrous iron (\(\mathrm{Fe}^{+2}\)) is more readily absorbed than ferric iron (\(\mathrm{Fe}^{+3}\)). Therefore, a low pH in the stomach does not inhibit but rather promotes iron absorption. This statement is not true. Based on the analysis of each option, the correct answers are A, B, and C.

Key concepts

Iron Uptake Regulation

Iron uptake in the human body is a critical process, as it is essential for producing hemoglobin, the protein that carries oxygen in the blood. The regulation of iron absorption is a finely tuned system that prevents both deficiencies and excesses of iron. This occurs predominantly at the level of the intestinal mucosal cells. These cells are located between the digestive lumen – where the food is present – and the blood vessels that will carry the absorbed nutrients away.

The mucosal cells use specific proteins to transfer iron from the intestine into the body. One principal protein is the divalent metal transporter 1 (DMT1), which transports ferrous iron (\( \text{Fe}^{+2} \) ) across the cell membrane. Another important component is hepcidin, a hormone produced by the liver that regulates iron egress from mucosal cells into the blood. High levels of hepcidin can inhibit iron absorption by degrading the iron exporter ferroportin.

Furthermore, internal body signals, such as the level of iron already stored in the body and the current need for iron, significantly influence mucosal iron uptake. For instance, when iron stores are low, the mucosal cells decrease hepcidin production, promoting more iron absorption. It is this precise interplay of factors that maintains iron homeostasis within the body.

Ascorbate and Iron Availability

Vitamin C, also known as ascorbic acid or ascorbate, plays a pivotal role in increasing the availability of iron in the digestive tract. Its primary action is to reduce ferric iron (\( \text{Fe}^{+3} \) ) to ferrous iron (\( \text{Fe}^{+2} \) ), which is the form more readily absorbed by the intestinal mucosa. This reduction is essential because non-heme iron, found in plant-based foods, is usually present in its ferric form, which is not as easily taken up by DMT1 transporters.

Ascorbate acts by binding to ferric iron and donating an electron, effectively reducing it. Additionally, ascorbate can also chelate iron, creating a complex that prevents it from being sequestered by other dietary factors that inhibit iron absorption, like phytic acid. Furthermore, the presence of ascorbate can counteract the negative effects of certain inhibitors of iron absorption, such as tannins found in tea. By consuming vitamin C-rich foods or supplements with meals, individuals can enhance their absorption of iron, which is particularly beneficial for those who follow a plant-based diet and might be at risk of iron deficiency.

Apoferritin Synthesis

Once iron is absorbed by the intestinal mucosal cells, it is critical to store it safely and prepare it for transport. This is where apoferritin comes into play. Apoferritin is the precursor to ferritin, the primary iron storage protein in cells. The synthesis of apoferritin is closely linked to the level of iron in the body. When iron levels in the mucosal cells rise after iron absorption, more apoferritin is produced to safely sequester the iron and prevent it from causing harm through oxidative damage.

The level of ferritin synthesis is, therefore, a reflection of the body's need for iron. In situations of iron deficiency, less ferritin is needed, and consequently, the synthesis of apoferritin decreases. Conversely, when iron is abundant, the production of apoferritin increases. This synthesis reflects an intelligent system whereby ferritin acts as a buffer against iron deficiencies and excesses, ensuring that the release of iron into the bloodstream is precisely matched to the body's demands. This regulation protects against iron-related pathologies and is critical for maintaining overall health.