Exogenous iron

The majority of body iron is not chelatable (iron from cytochromes and hemoglobin). There are two major pools of chelatable iron by DFO (19). The first is that delivered from the breakdown of red cells by macrophages. DFO competes with transferrin for iron released from macrophages. DFO will also compete with other plasma proteins for this iron, when transferrin becomes saturated in iron overload. The quantity of chelatable iron from this turnover is 20mg/day in healthy individuals and iron chelated from this pool is excreted in the urine (19). The second major pool of iron available to DFO is derived from the breakdown of ferritin and hemosiderin. The ferritin is catabolized every 72 hours in hepatocytes, predominantly within lysosomes (I). DFO can chelate iron that remains within lysosomes shortly after ferritin catabolism or once this iron reaches a dynamic, transiently chelatable, cytosolic low-molecular-weight iron pool (20). Cellular iron status, the rate of uptake of exogenous iron, and the rate of ferritin catabolism are influent on the level of a labile iron pool (21). Excess ferritin and... 

The catalytic effect of iron on enhancing the rate of reduction of Cr(Vl) by human microsomes has been reported earlier (Myers and Myers 1998). Various forms of exogenous iron markedly enhanced both liver and lung microsomal rates of Cr(VI) reduction. Small increases in intracellular iron have shown to cause large increases in in the rate and extent of Cr(Vl) reduction. Thus, individuals exposed simultaneously to Cr(VI) and agents that may increase intracellular iron could, therefore, be at potentially greater risk for toxicity and carcinogenicity of Cr(VI). 

There are grounds to speculate that similar effect, namely, the appearance in the culture medium of significant amounts of free NO released from rapidly decomposing DNIC under the action of exogenous iron chelators was responsible for apoptosis induction in HeLa cells by DNIC -1- chelators. 

Subcutaneous apphcation of Fe-citrate (Fe doses of 120 and 240 pM/kg mouse) inhibited iNOS expression after a simultaneous intravenous injection of 6 mg Escherichia coli hpopolysaccharide per mouse (Komarov et al. 1998), while exogenous iron did not affect systemic NO levels when given at 6 h after LPS injection, i.e. after iNOS expression (Komarov et al. 1997). In exercised (after a training period of 30 and 60 min, swinuning for 120 min per day for 3, 6, and 12 months, respectively) rats, plasma nitric oxide and iron concentrations were negatively correlated (Xiao and Qian 2000). 

Iron is a vital constituent of many bacterial enzyme-systems. Most micro-organisms have evolved high-affinity pathways for the assimilation of Fe(III), which utilise low-molecular-weight carriers or siderophores (iron-tearers). A carrier is essential to iron accumulation since very little of it is available in aerobic environments. The problem is not in the main caused by low exogenous iron levels, indeed iron is the foiuth most... 

Figure 1, The Growth of Es h rj chia co li 0111 in Human Milk in the Presence and Absence of Exogenous Iron, Open Markers—Milk Samples Without Exogenous Iron, Closed Markers—Milk Samples with Exogenously Added Iron. Reprinted with Permission from Bullen et al. (1972), Copyright by the British Medical Association.

High-resolution ENDOR of iron-NO complexes has proven ideal for resolving questions about the relative orientations of exogenous iron ligands in facial triad oxygenases. Because this volume has a chapter devoted to recent ENDOR studies (see Chapter 3), only a brief account of one example, in which an Fe-NO complex... 

The ability of the enzyme-bound iron to exchange with exogenous iron is very slight except during enzyme activity, and the extent of the exchange is a function of the amount of reaction catalyzed for example, both the rate of reaction and the rate of ion exchange increase with temperature and with time (Tokuyama, 1959a). 

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