Iron utilization

The most common method of converting iron ore to metallic iron utilizes a blast furnace wherein the material is melted to form hot metal (pig iron). Approximately 96% of the world s iron is produced this way (see Iron). However, in the blast furnace process energy costs are relatively high, pollution problems of associated equipment are quite severe, and capital investment requirements are often prohibitively expensive. In comparison to the blast furnace method, direct reduction permits a wider choice of fuels, is environmentally clean, and requires a much lower capital investment. 

Zinc protoporphyrin IX is a normal metabolite that is formed in trace amounts during haem biosynthesis. However, in iron deficiency or in impaired iron utilization, zinc becomes an alternative substrate for ferrochelatase and elevated levels of zinc protoporphyrin IX, which has a known low affinity for oxygen, are formed. This zinc-for-iron substitution is one of the first biochemical responses to iron depletion, and erythrocyte zinc protoporphyrin is therefore a very sensitive index of bone-marrow iron status (Labbe et ah, 1999). In addition, zinc protoporphyrin may regulate haem catabolism by acting as a competitive inhibitor of haem oxygenase, the key enzyme of the haem degradation pathway. However, it has been reported... 

MacCartney, A. P. and Mack, D. J., Iron utilization by Thule Eskimos of Central Canada, American Antiquity. 38(3), 328-338 (1973). 

Table III. Effects of Soy Protein on Iron Utilization in Humans.

Figure 8.4 Model of Fur and RyhB interaction to regulate iron utilization. (From Masse and Gottesman, 2002. Copyright (1993) National Academy of Sciences, USA.)...

The iron responsive element, a critical factor in the control of proteins involved in iron utilization, has been identified as the cytoplasmic form of the iron-sulfur protein aconitase (Kennedy et al., 1992). Activated macrophages have been shown to activate this element, presumably by attack of the iron-sulfur cluster by NO (Drapier et al., 1993). It has been claimed that this attack is mediated by peroxynitrite (Castro et al., 1994 Hausladen and Fridovich, 1994, but this conclusion is not universally accepted. 

Ecelbarger CA, Greger JL. 1991. Dietary citrate and kidney function affect aluminum, zinc and iron utilization in rats. JNutr 121 1755-1762. 

Most patients with Al intoxication develop an erythropoietin-resistant microcytic anemia in the absence of iron deficiency, and this may be a useful early indication of Al toxicity [41,93,254,255]. The chemical similarity between Fe3+ and Al3+ suggest that both elements will have similar metabolic effects, suggesting that iron and Al compete during erythropoiesis, resulting from a reversible block in heme synthesis due either to a defect in porphyrin synthesis or to impaired iron utilization. It was also suggested that the main mechanisms for Al toxicity in the erythropoietic system are the interference of Al in the uptake and utilization of iron and an interaction of Al with cellular membrane components, affecting not only their structures but also their functions [256]. 

We conclude that plural mechanisms exist for siderophore iron utilization in the enteric bacteria. The iron may be rapidly removed with ( . coli) or without (S. typhimurium) effective transport of the ligand. The rate of this process is such that labilization of the iron by reduction appears most likely. The intact ferric chelates also pass the cell envelope, but by a generally slower mechanism. An estimate of the number of atoms of iron acquired per bacterium indicates true uptake rather than adsorption to the cell surface has taken place. In both organisms the A-cis chromic coordination isomer of ferrichrome is active, indicating that dissociation and/or isomerization is not obligatory for its transport. 

The active transport aspect of siderophore iron utilization remains largely unexplored, although such a process probably exists—in addition to facilitated diffusion—in view of the high affinity of the cells for siderophores and the likely participation of an energized state of the membrane in their transport. Experiments with whole cells must perforce be performed with mutants lacking the ability to make these carrier molecules. 

Powers HJ, Weaver LT, Austin S, Wright AJ, and Eairweather-Tait SJ (1991) Riboflavin deficiency in the rat effects on iron utilization and loss. British Journal of Nutrition 65,487-96. 

Neutron activation analysis has been applied in studies of plasma clearance of 58pe iron utilization in pregnant... 

Iron toxicity can be expected if the amount of free iron released into the plasma exceeds the plasma iron-binding capacity. This is more likely to occur when using iron sorbitol-citric acid complex (iron sorbitex), since the iron is less firmly bound than with iron dextran. Several conditions associated with low iron-binding capacity, such as malnutrition (kwashiorkor, malnutrition syndrome) and previous or simultaneous oral iron therapy appear to predispose to the development of these toxic reactions. In addition, folic acid deficiency has been reported to be a predisposing factor (SED-9, 516), the likely mechanism being altered iron utilization secondary to folic acid deficiency, which results in an increased saturation of ironbinding capacity. 

Iron Utilization. Iron deficiency, a major cause of anemia in humans, is a world-wide problem (392,393,394) and the search for... 

The bioavailability of iron from any source (e.g., iron supplement, food or meal composite) is considered to be that portion of the total iron which is metabolizable. Philosophically, this concept is important because the amount of iron utilized by avian and mammalian species is directly associated with iron need. When assaying iron bioavailability, it is therefore necessary to use an organism whose need will exceed the amount provided. In animal assays of iron bioavailability, iron need is assured by a growth phase and/or creation of iron deficiency through feeding an iron deficient diet and phlebotomy. Because healthy subjects are usually used in human assays of iron bioavailability (Cook et al., 1981 Cook and Monson, 1976 Radhakrishman and Sivaprasad, 1980), it is inappropriate to compare the data obtained from animal and human assays. In fact it is questionable if assays of iron bioavailability yield good information on the quantities of metabolizable iron available when healthy human subjects are used. 

Only a few investigators have compared the effects of various forms of phosphorus on zinc and iron utilization by animals. 

The effect of various forms of phosphorus salts on zinc and iron utilization in men have not been assessed. Differences in the cecal lora growth of rats and men could result in differences between the two species in their ability to hydrolyze polyphosphates (33. 34). Thus, at this time it is difficult to speculate whether equal quantities of orthophosphates and polyphosphates in the diet would have different effects on zinc and iron utilization by human subjects. 

The levels of many other compounds (i.e. ascorbic acid, protein and calcium) in the diet can moderate the effects of phosphorus on zinc and iron utilization. Probably the most important of these factors is calcium. If both inorganic calcium and phosphorus salts are added to a diet, the bioavailability of iron and probably zinc from that diet will be depressed probably. 

Further studies of the effects of dietary fiber from various sources upon iron utilization by human subjects are necessary. Some existing studies are inconclusive because of their short duration others because of the small samples studied. Long term studies of the fiber-rich, low energy diets of many less developed regions would also be important for evaluation of the iron deficiency that often prevails. 

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