Iron excretion

Weintraub, L.R., Demis, J., Conrad, M.E. and Crosby, W.H. (1965). Iron excretion by the skin. Selective localization of iron epithelial cells. Am. J. Pathol. 46, 121-127. 

These different systems come into operation under different conditions both environmental and in terms of growth requirements. As we will see later in this chapter, yeasts do not appear to have a mechanism for iron excretion, so that their cellular iron homeostasis, as in E. coli, relies on tight control of uptake and eventually storage. As we will see when we examine these iron uptake systems in detail, most of them require ferrous iron, rather than ferric. This implies that the first step required for iron transport is the reduction of Fe3+ to Fe2+ by membrane-bound reductases. 

Iron is an essential element, for humans and for many forms of life, but even a modest excess can be toxic as the human body does not have an effective iron excretion mechanism. It is therefore necessary to maintain an appropriate level of iron in the body, to supply iron in absorbable form if it is deficient (anemia) and to remove iron if present in excess. Inorganic coordination chemistry plays an important role in dealing with these complementary conditions of deficiency and of excess. The latter condition is much more common than often supposed, for there are a number of conditions, such as hemochromatosis and thallasemia, where the build-up of iron in essential organs is eventually lethal. Mild iron poisoning is not infrequent in children, while even iron fortification of foodstuffs can have adverse effects. Mild iron poisoning can be treated with bicarbonate or phosphate, which presumably complex and precipitate the iron. ... 

To enhance iron excretion, intensive chelation therapy is used. The most successful drug is desferrioxamine B, a powerful Fe3+-chelator produced by the microbe Streptomyces pilosus,6 The formation constant for the Fe(III) complex, called ferrioxamine B, is 103afi. Used in conjunction with ascorbic acid—vitamin C, a reducing agent that reduces Fe3+ to the more soluble Fe2+— desferrioxamine clears several grams of iron per year from an overloaded patient. The ferrioxamine complex is excreted in the urine. 

Clinical uses of atomic absorption spectroscopy in the analysis for iron have not yet been published and the low iron levels in most biological fluids may very well be limiting. An interesting clinical application was demonstrated by Briscoe (B8), who determined by atomic absorption spectroscopy iron excretion in the urine of a patient treated with desferrioxamine for hemochromatosis. 

Prolonged heavy excess of iron intake overwhelms the mechanism described and results in haemo-siderosis, as there is no physiological mechanism to increase iron excretion in the face of increased absorption. Iron-deficient subjects absorb up to 20 times as much administered iron as those with normal stores. Abnormalities of the small intestine may interfere with either the absorption of iron, as in coeliac disease and other malabsorption syndromes, or possibly with the conversion of iron into a soluble and reduced form, e.g. following loss of acid secretion after a partial gastrectomy. 

Method After emptying the bladder, deferoxamine (one vial of 500 mg) is injected (i.m.) and urine is collected for exactly 6 hours with subsequent determination of iron excretion. Iron levels of > 4 mg are considered to be characteristic of primary haemochromatosis, while iron levels of <2 mg are either regarded as normal or caused by secondary haemosiderosis. This test can also be executed as follows 10 mg/kg BW deferoxamine (i.m.) with urine collection for 24 hours, whereby haemochromatosis value is > 10 mg iron and normal value is < 2 mg. 

While the deferoxamine test (s. p. 99) is often considered obsolete, it can nevertheless serve as another stone in the mosaic and prove helpful in the diagnostics or follow-up of HC, since it is an iron chelation test that is easy to apply, free of side effects and inexpensive. In healthy persons, this test reveals a urinary iron excretion of <1 — 2 mg in haemosiderosis, the excreted amount is <4 mg, and in HC >4 mg. (461)... 

Excess iron can be removed by either phlebotomy (letting of blood from a vein) or administration of the chelating agent, deferrioxamine, for cases of chronic excess iron. Ascorbic acid can accelerate iron excretion about twofold. 

Iron is a major component of the Earth s crust, but its own chemistry greatly limits utilization and also sets the basis for its toxicity. The capacity of readily exchanging electrons in aerobic conditions makes iron essential for fundamental cell functions, such as DNA synthesis, transport of oxygen and electrons, and cell respiration. However, because humans have no means to control iron excretion, excess iron, regardless of the route of entry, accumulates in parenchymal organs and threatens cell viability. 

Gomes J, Lloyd OL, Norman NJ and Pahwa P (2001) Dust exposure and impairment of lung Junction at a small iron foundry in a rapidly developing country. Occup Environ Med 58 656-662. Green R, Charlton R, Seftel R, Bothwell TH and Maget E (1968) Body iron excretion in man. A collaborative study. Am J Med 45 336-353. Guerinot ML and Yi Y (1994) Iron nutritious, noxious, and not readily available. Plant Physiol 104 815-820. 

Urinary and Fecal Iron Excretion Promoted by Chelating ... 

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