Summary

These notes discuss the trace element iron, its dietary sources, absorption mechanisms, and the regulatory processes involved in its uptake. It describes iron's roles in the body, its transport and storage forms, and abnormalities associated with iron metabolism, such as deficiency and overload. Topics covered include absorption, distribution, and regulation of iron in the body, highlighting various factors impacting these processes.

Full Transcript

# TRACE ELEMENTS ## IRON ### Dietary Sources: - The liver, heart, kidney, spleen, meat and egg yolk are very good sources of iron. - Molasses, dates, legumes, vegetables and whole cereals are good sources. ### Absorption: - variable and dynamic process - in the duodenum and upper jejunum - The am...

# TRACE ELEMENTS ## IRON ### Dietary Sources: - The liver, heart, kidney, spleen, meat and egg yolk are very good sources of iron. - Molasses, dates, legumes, vegetables and whole cereals are good sources. ### Absorption: - variable and dynamic process - in the duodenum and upper jejunum - The amount of iron absorbed compared to the amount ingested is typically low, but may range from 5%-35% ### Factors Influence Iron Absorption: - **Ascorbate and Citrate:** Increase iron uptake in part by increasing the solubility of the metal in the duodenum. - **Phytates in Wheat and Some Other Cereals and Tannins in (Non-herbal) Teas:** Decrease the solubility of iron; thus inhibiting its absorption. ### Mechanism: - A ferric reductase enzyme on the enterocytes' brush border and Duodenal Cytochrome b (DCYTB), reduces ferric Fe3+ to Fe2+. - Ferrous ions are transported across the enterocyte apical membrane by The Divalent Metal Transporter 1 (DMT1), (a proton coupled divalent ion transporter. - Iron effluxes from the enterocyte basolateral membrane through ferroportin and is oxidised by a membrane bound ferroxidase, hephaestin, yielding ferric ions that are then bound by plasma transferrin for distribution around the body via the blood. ### Regulation Of Iron Absorption: - **Principle Regulatory Mechanism:** Involves sensing of high body iron stores or low erythroid iron requirements by the liver, which produces an inhibitory peptide, hepcidin, that acts on the intestine to decrease iron absorption. - **Dcytb and DMT1 levels:** Are also affected, most likely in response to altered iron levels in enterocytes caused by hepcidin's action on iron efflux through ferroportin. ### Distribution And Functions: - The total iron in the body is about 4g. It is present in the body in the 2 forms: 1. **Functional Forms (75%)** - These are mostly in the form of *hemoproteins* such as *hemoglobin*. 2. **Nonfunctional Forms (25%)** - These are transport and storage forms of iron. - They are *non-hememetalloproteins*. - **Transferrin:** This is the *transport* form of iron in the blood plasma. - **Ferritin:** This is the chief *storage* form of iron in the tissues. It is present in the liver, kidneys, spleen, bone marrow, and intestinal mucosal epithelium. - **Hemosiderin:** This is present in iron stores when the body contains excess iron. - **Lactoferrin:** It is present in milk; it contains iron that is bound to a *glycoprotein*. It facilitates iron transport and storage in milk ### Blood Iron: 1. **In Red Cells:** The erythrocytes contain hemoglobin, which contains 3.4 mg of iron per gram. 2. **In Plasma:** - **Transferrin:** The plasma iron concentration is 50-150 µg/dL. Iron is carried by a glycoprotein, transferrin, which carries 2 atoms of ferric iron per molecule. - It is synthesized in the liver. - Low degree of transferrin saturation by ion facilitates iron release from the mucosal cells. - **Total Iron-Binding Capacity (TIBC):** Transferrin may carry up to 250-400 µg of iron per dL plasma. This means that, on the average, only about 30% of the TIBC is saturated. - **Unsaturated Iron-Binding Capacity (UIBC):** About 60-70% of transferrin is unsaturated. - **Iron Deficiency Anemia:** The plasma iron decreases while the TIBC tends to increase. - **Ferritin:** Plasma contains very low concentrations of ferritin, which is a very good index of iron storage. It decreases in iron deficiency and increases in hemosiderosis. ### Abnormalities Of Iron Metabolism: #### I. Iron Deficiency Anemia - **Characteristics:** Microcytic and hypochromic red blood cells. Excess menstrual flow or gastrointestinal bleeding. - **Treatment of Iron Deficiency Anemia Includes:** - Treatment of the cause of bleeding. - A preparation of iron (iron dextran) for intramuscular injection has been used in patients who cannot tolerate or absorb oral iron. - **Caution must be taken when iron is given parenterally because of the possibility of oversaturation of tissues with resultant production of hemosiderosis.** #### II. Iron Toxicity (Hemosiderosis or Hemochromatosis) - **The body is unable to excrete a large load of iron. Iron differs from most other minerals in that its quantity in the body is controlled by regulating its absorption rather than excretion.** ##### Causes: - In patients of aplastic or hemolytic anemia who have received many blood transfusions over a period of years. - Inherited anomaly of iron absorption, some persons has excessive ability to absorb iron which produces iron accumulation after many years. - Overdose of parenterally administered iron. - **In all above conditions, hemosiderin accumulates in different tissues, a condition known as hemosiderosis.** ### Hemochromatosis - **Hemosiderosis** with injury to involved tissues as manifested by cellular degeneration and **fibrosis**. - **Clinical manifestations:** Include *bronzed pigmentation of the skin, liver cirrhosis and pancreatic fibrosis, leading to diabetes mellitus (bronze diabetes)*. - **Serum iron** is elevated and **transferrin** becomes 70-90% saturated with iron. ## IODINE ### Dietary Sources: - The best sources are *seafood*. Vegetables and fruits grown near seaboard contain high concentrations of iodine. Iodized table salt is now available to prevent iodine deficiency. ### Absorption And Distribution: - *Organic iodine* is partly converted to *inorganic iodide* before absorption. Inorganic iodine ($I_2$) and iodide ($I^{-}$) are absorbed via skin, lungs and intestine. ### Distribution: 1. **Thyroid Gland (30%-50%)** - Concentrate iodide from the blood. *Thyroglobulin* contains iodide in the form of monoiodotyrosine (MIT), diiodotyrosine (DIT), triiodothyronine ($T_3$) and tetraiodothyronine or thyroxine ($T_4$), mostly the last two. 2. **Other tissues and body fluids (50%-70%)** - Iodide is partly in organic combination, $T_3$ and $T_4$ and *their metabolites*, and partly in the form of inorganic iodide (NaI and KI). Inorganic iodide markedly decreases in iodide deficiency. ### Functions: - Thyroid hormones. ### Excretion: 1. **In urine (70%)**: This is mainly in the form of *inorganic iodine*. - $T_3$ and $T_4$ are *not* present normally in urine being transported in conjugation with plasma proteins. 2. **In feces (30%):** This represents the *unabsorbed* iodine of diet and iodine excreted in saliva, bile and intestinal secretions. ### Iodine Deficiency: - Thyroid hypertrophy (*goiter*) occurs if iodine deficiency is prolonged.

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