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Phosphorus And Iron: Nutritive Significance, Clinical, Deficiencies And Biological Value As Mineral Supplements

Updated on February 23, 2014

Bone Pains In Hypophosphatemia

Hypophosphatemia leads to weakness, anorexia, malaise and bone pains. Hyperphosphatemia per se does not produce any adverse symptoms, but prolonged hyperphosphatemia together with hypercalcemia results in metastatic calcifications.
Hypophosphatemia leads to weakness, anorexia, malaise and bone pains. Hyperphosphatemia per se does not produce any adverse symptoms, but prolonged hyperphosphatemia together with hypercalcemia results in metastatic calcifications. | Source

Phosphorus

Most of the phosphorus (85%) in the body is present in bones and teeth. In all tissues, this element is present intracellularly as phosphates. The total body content of phosphorus is 800 to 900g. In the plasma, it occurs as inorganic orthophosphate at a concentration of 2.8 to 4 ng/dl. Around 88% of phosphaorus is in ionic form and the rest is present in the protein- bound form. Phosphorus is widely distributed in dietary articles and hence dietary deficiency is rare. Though, the exact requirement of phosphorus has not been determined, probably it is the same as calcium. Dairy products, eggs, cereals and meat are rich sources.

About 80 to 90% of ingested phosphorus is absorbed. The serum level is controlled mainly by the renal excretory mechanism. Around 85% of filtered phosphate is absorbed at the proximal tubule and only 10 to 15% is lost in urine. Negative phosphate balance is usually casued by the abnormalities of renal clearance. In renal failure, serum phosphate goes up and in renal tubular dysfunctions, it may fall. Aluminium hydroxide binds phosphates and makes it unasorbable so that in prolonged antacid therapy, phosphorus absorption may suffer. Hypophosphatemia leads to weakness, anorexia, malaise and bone pains. Hyperphosphatemia per se does not produce any adverse symptoms, but prolonged hyperphosphatemia together with hypercalcemia results in metastatic calcifications.

Iron Storage In Bone Marrow

 Iron also exists in combination with the Iron storage proteins as ferritin and hemosiderin, in the macrophages seen in the muscles, liver and bone marrow. Stored Iron is demonstrable by Prussian blue reaction histochemically. Stored Iron available f
Iron also exists in combination with the Iron storage proteins as ferritin and hemosiderin, in the macrophages seen in the muscles, liver and bone marrow. Stored Iron is demonstrable by Prussian blue reaction histochemically. Stored Iron available f | Source

Iron

The total content of Iron in healthy adults is 4.2g. Of this, 58 to 66% is present in hemoglobin. Part of the Iron is present in myoglobin. Iron also exists in combination with the Iron storage proteins as ferritin and hemosiderin, in the macrophages seen in the muscles, liver and bone marrow. Stored Iron is demonstrable by Prussian blue reaction histochemically. Stored Iron available for erythropoiesis is about 1.2 to 2g. Tissue Iron is mainly present in enzymes. This amounts to 300 mg and is not available for erythropoiesis. Total plasma Iron is 3 to 4 mg and the levels range from 80 to 120 ug/dl. Animal foods like meat, liver, kidney, fish and egg yolk are rich in Iron. Vegetable sources are green vegetables and fruits, Onions, cereals, pulses, oil seeds, jiggery, raisins, grapes, apricots and dates. The daily average intake of Iron is 10 to 20 mg, out of which 1 to 2 mg is absorbed. Significant amounts of Iron may be obtained from water sources and from Iron cooking vessels. The bioavailability of Iron in the average African diet is low. Milk is a poor source of Iron and hence babies fed solely on unfortified milk develop Iron deficiency within 6 to 12 months. Iron from animal foods is absorbed better (11 to 22%) than that from vegetable sources (1 to 7 %).

© 2014 Funom Theophilus Makama

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