Iron Metabolism PDF

Iron metabolism Overview Introduction Distribution of iron in the body Biochemical function Requirements Iron metabolism Disorders of iron metabolism Introduction  A trace element is a dietary element that is needed in very minute quantities for the prope...

Iron metabolism Overview Introduction Distribution of iron in the body Biochemical function Requirements Iron metabolism Disorders of iron metabolism Introduction  A trace element is a dietary element that is needed in very minute quantities for the proper growth, development, and physiology of the organism.  Iron is the most important trace element. Distribution of iron in the body  Biochemical functions 1. Required for synthesis of – Hemoglobin, – Myoglobin, – Cytochromes (ETC), – Peroxidase (phagocytosis). 2. Essential for synthesis of non heme iron (NHI) compounds like, Succinate dehydrogenase. Iron-sulfur proteins. 3. Iron is associated with effective immuno-competence of body.  15-20 mg /day, only 2 mg is absorbed normally  Sources if Iron The best sources of iron are found in, meat, eggs, salmon, tuna, liver, poultry. Smaller amounts of iron are found in dark leafy greens, such as spinach, fruits(apples) and whole grains. Iron is better absorbed from animal than vegetable sources. Factors That Influence Iron Absorption 1-Reducing agents that help reduction of iron to ferous (Fe+2): Ascorbic acid, citrate, Sh- containing a.a., Facilitators Hcl of the stomach. 2-↑Body requirement→↑rate of absorption Phytates (in cereals), Inhibitor Oxalates, tannic acid, antacids s Calcium, manganese, zinc Competito rs Iron metabolism  In case of non heme iron, most Iron in the plant food is in the ferric form( Fe+3 ), but Iron can only be absorbed by the bowel in divalent form(ferrous.,Fe2+). For this reason, reducing agents in food such as ascorbic acid (vitamin C ) promote iron uptake. Firstly it should be reduced from Fe+3 to Fe+2 by reductase agent (ferric reductase Dcytb1 ). After that it will be transport to inside the enterocyte by divalent material transport ( Dmt1 ). when heme iron ingested, it will be absorbed quickly because of appearance of Heme Carrier Protein( HCP) in the apical part of enterocyte.  Iron enter the enterocyte: 1-some will be temporary stored in the enterocyte as ferritin. 2-some will transport through the basolateral surface of enterocyte by ferroprotein. Hephaestin is membrane bound- ferri oxidase enzyme, which converts Fe2+ to Fe3+ at the basal surface prior to binding apotransferrin. Storage form of Iron in body Transferrin :( protein carrier ) of Iron in the circulation (e.g from git →BM) Apotransferrin: ( transferrin not bind to Iron) Ferritin : storage form of Iron in the hepatocytes and enterocytes. Hemosedrin: aggregated ferritin overloaded with iron  Iron transport-Transferrin  Iron is carried in Fe3+ state bound to a specific iron transport protein known as transferrin.  transferrin are iron-binding plasma glycoproteins that are synthesized in the liver.  Each transferrin can carry 2 (Fe3+) ions.  Normally,1/3 of circulating transferrin is completely saturated with 2(Fe3+),while the other 2/3 molecules contain only 1 (Fe3+) or no (Fe3+).  The transferrin–iron complex enters the cell through specific receptors and the iron ions are released for  When iron stores become low, transferrin levels will increase.  When there is too much iron, transferrin levels are low  The total iron binding capacity of transferrin is 300Mg/dl plasma.  This TIBC is increased with iron defeciency anaemia→(empty transferrin due to iron defeciency).  While, TIBC is decreased with hemolytic anaemia →↑saturation of transferrin with iron which is released from hemolysed cells.  Ferritin  Ferritin is the primary iron storage protein.  It is present in intestinal mucosa ,liver, spleen,BM.  Apoferritin can uptake up to 4000 iron atoms to give ferritin.  It has the ability to gain and release iron according to iron stores. Hemosiderin It is formed by partial degradation of ferritin due to overloading of ferritin with iron Present in liver, spleen & bone marrow. Hemosiderin accumulates forming brown aggregates when iron levels are increased In tissues.  Iron level in blood  It is important to measure iron and iron-binding capacity to detect iron deficiency or overload.  Serum iron on its own provides no complete information on iron level. What tests are used ? Total iron- Serum Iron Serum binding ferritin capacity Total iron-binding capacity It is a medical laboratory test that measures the blood's capacity to bind iron with transferrin. It is measuring the maximum amount of iron that it can carry, which indirectly measures transferrin It is calculated by adding serum iron and unsaturated iron binding capacity (UIBC) It is most frequently used along with a serum iron test to evaluate people suspected of having either iron deficiency anemia or iron overload. Serum Iron, TIBC, UIBC Total iron-binding capacity Blood Unsaturated Serum serum iron Iron binding  Disorders of iron metabolism Iron defeciency anaemia. Iron overload Causes: (Hemosiderosis) Inadequate intake, Causes: Impaired absorption, Repeated attacks of hemolysis, Chronic blood loss & Increased demand. repeated blood transfusion. Accumulation of hemosiderin in liver & other reticulo-endothelial system. (Hemochromatosis): In liver, hemosiderin deposit leads to cirrhosis. Pancreatic cell death leads to diabetes. Deposits under skin cause yellow-brown Laboratory findings: discoloration, called hemochromatosis. 1. Serum Laboratory findings: 1. Serum iron level is increased iron level is decreased 2. TIBC is decreased 2. TIBC is increased 3. Ferritin level is increased 3.