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PubMed1987

The fate of iron compounds in the gastrointestinal tract. Coordination-chemical facts.

Simple ferrous salts are sources of ferric species emerging from the hydrolysis induced by oxidation in the gastrointestinal tract. Ferric ions from simple ferric salts undergo hydrolysis at an early stage succeeding oral administration. The hydrolysis products from either type of sources are ill-defined. Recent progress in the understanding of iron(III) hydrolysis shows that small polynuclear hydroxo complexes can be prepared, which are well-defined and susceptible to uptake by mucosal proteins.

Animals↗
PubMed1990

Lipid peroxidation effects of a novel iron compound, ferric maltol. A comparison with ferrous sulphate.

Lipid peroxidation effects of ferric maltol have been compared with those of ferrous sulphate both in lecithin liposomes and in brush border and mitochondrial membranes prepared from rat small intestine. Ferrous sulphate, but not ferric maltol, initiated peroxidation in liposomes as measured by conjugated diene production, but, with 500 microM ascorbic acid present, both caused intense peroxidation which was inhibitable by N2, tocopherol, maltol and ferrous chelators, but not by OH or H2O2 scavengers. The rate of peroxidation increased with ferrous sulphate concentration up to 100 microM but was independent of ferric maltol concentration between 5-500 microM. Material eluted from rat small intestine contained a reducing factor, similar in size to ascorbic acid, capable of generating ferrous ions from ferric maltol and initiating peroxidation. Peroxidation in mitochondrial membranes appeared unaffected by addition of iron whilst that in brush border membranes was detectable only in the presence of iron. At iron concentrations of 100 microM and above ferric maltol produced less liposomal peroxidation than ferrous sulphate. Maltol itself may delay recycling of Fe3+ to Fe2+. Thus ferric maltol could provide a less toxic alternative to ferrous salts in the oral treatment of iron-deficiency.

Animals↗
PubMed1986

Effect of iron compounds on antibacterial function of human polymorphs and plasma.

Human plasma was bactericidal for small numbers of Klebsiella pneumoniae, but larger numbers grew slowly over a period of 24 h. Human polymorphs in a clot of autologous plasma had a bacteriostatic effect on relatively large numbers of bacteria for up to 24 h and were much more effective than plasma alone. The bactericidal effect of plasma could be abolished by saturating the plasma albumin and hemopexin with hematin, the haptoglobin with hemoglobin, and the transferrin with Fe3+. Stimulation of bacterial growth in the presence of polymorphs depended on the degree of saturation of the plasma proteins which bind the Fe3+ or heme compounds. Hematin bound to albumin appeared to be readily available to K. pneumoniae. Free hemoglobin stimulated bacterial growth but the organism could not utilize the haptoglobin-hemoglobin complex. In the presence of polymorphs the addition of Fe3+ to give 60% saturation of the transferrin with iron led to rapid growth after a long delay (19 h). Progressive increases in saturation above 60% gave correspondingly quicker growth, suggesting that the higher the saturation of transferrin, the easier it is for the bacteria to acquire iron. The antibacterial effect of the plasma appears to be critically dependent on the availability of iron for the bacteria, and this in turn affects the ability of the polymorphs to control bacterial growth.

Blood Bactericidal Activity↗