Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Iron Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources

Evidence for regulatory control of iron uptake from ferric maltol across the small intestine of the rat.

1. 59Fe absorption from the novel iron compound, ferric maltol, was studied in rats pretreated twice daily for two weeks with non-radioactive ferric maltol in oral doses containing 7 mg elemental iron. Tissue accumulation of 59Fe 2 h after administration of radioactive ferric maltol into the stomach was significantly lower in iron pretreated animals than in saline-treated controls. 2. 59Fe uptake from ferric maltol into isolated fragments of ileum and of duodenum was of similar magnitude in control animals but in iron-treated animals, duodenal uptake was significantly lower than that of the ileum. 3. Absorption of 59Fe was also investigated in anaesthetized rats after intestinal perfusion with saline (controls) or with 5 mM chenodeoxycholate to render the intestines more permeable. 4. Changes in permeability of the small intestine were monitored by estimating the amount of [14C]-mannitol absorbed and fluid secreted with reference to the non-absorbable [3H]-inulin in the perfusate effluents. 5. Despite the increased permeability of the intestines after bile salt treatment, there was little difference from control in the tissue accumulation of 59Fe from ferric maltol 2 h after intraduodenal administration. However 59Fe absorption from ferrous sulphate was significantly increased after bile salt treatment. 6. Gel filtration profiles of plasma made 5 and 60 min after intraduodenal administration of [59Fe]-ferric [3H]-maltol demonstrated that metal and ligand do not enter the circulation as the complex even when intestinal permeability is increased. 7. Uptake of 59Fe was investigated in isolated fragments of rat small intestine after saline or bile salt perfusion. Although 59Fe uptake from ferric maltol was somewhat greater in the bile salt-treated intestinal fragments, saturable kinetics were still observed. By contrast, "Fe uptake from ferrous sulphate: ascorbate was greatly enhanced by bile salt pretreatment and a very large diffusional component of uptake was evident. 8. It is concluded that iron uptake from ferric maltol may well be under endogenous regulatory control even in damaged intestines, so it is unlikely that this novel iron compound can bring about iron overload when administered orally.

Animals↗

The development of awareness of the carcinogenic hazard of inhaled iron.

Numerous studies have observed that workers in ferriferous industries have an elevated risk of respiratory tract neoplasia. Research at the cellular and animal model levels indicates that iron compounds, per se, are carcinogenic. However, some investigators have suggested that inhaled iron compounds are merely carriers of other carcinogens. Evidence is presented that iron apparently is a principal carcinogenic hazard in inhalation of silicon dioxide, asbestos, and tobacco smoke. Included in the discussion are unresolved questions concerning the precise role of inhaled iron as a carcinogen.

Animals↗

Assmilation of iron by pathogenic Neisseria spp.

Iron assimilation by Neisseria meningitidis and Neisseria gonorrhoeae has been shown to be important to their growth and virulence. Iron acquisition in vitro was studied in an agar diffusion assay employing the iron-binding protein conalbumin. The ability of various iron compounds to alter the growth-inhibitory effect of conalbumin was investigated. On an equimolar iron basis, citrate-containing iron compounds were most effective; hemin was slightly less effective; ferrous sulfate and ferrous ammonium sulfate were even less effective; and the ferric compounds, ferric nitrate, ferric chloride, and ferric dextran (Imferon), were least effective. The results suggested that, as with Escherichia coli and certain other bacteria, the Neisseria spp. may utilize a citrate-mediated iron transport system. Microbial siderophores were also tested for their ability to relieve the growth-inhibitory effect of conalbumin. Two phenolate siderophores and Desferal enhanced growth inhibition in the deferrated form, but were inactive in the ferrated form. Several trihydroxamates of the ferrichrome family and coprogen were inactive in either the deferrated or ferrated forms. Of the 12 different siderophores tested, only the dihydroxamates (schizokinen, arthrobactin, and aerobactin) were stimulatory, but then only in the ferrated forms. Apparently, even though those siderophores could be utilized as specific iron transport agents by the Neisseria spp., they could not compete with conalbumin for iron under these assay conditions.

Conalbumin↗

Fortification of the diet as a strategy for preventing iron deficiency.

Progress in the fortification of food with iron is reviewed in the light of the different circumstances prevailing in the developed and developing world. Although fortification programmes are well established in developed countries many were not based on sound principles and there is no good evidence that they have proved effective. The important steps in establishing a fortification programme include accurate establishment of the need for iron fortification in a particular group or population, the choice of an appropriate combination of food vehicle and iron compound which is both stable and acceptable, and confirmation that the iron in the chosen blend is bioavailable and in different dietary settings. Only after the successful completion of controlled field trials using the chosen combination is the establishment of a regional or national fortification programme worthwhile. These points are illustrated by the success of field trials in the developing world, at least one of which has led to the implementation of a national programme directed to infants and children. Finally, a case study is described in which these principles were followed in the planning and execution of a successful field trial in an iron deficient Indian population in South Africa. The vehicle was curry powder and the iron compound Fe(111)EDTA.

Adolescent↗

The composition and the structure of bacterioferritin of Escherichia coli.

Bacterioferritin isolated from Escherichia coli is of two kinds: a protein containing a polynuclear iron compound, the bacterioferritin proper and a protein free of the polynuclear iron compound, the apo-bacterioferritin. Bacterioferritin of both kinds is characterized by absorption maxima at 417,530 and 560 nm, contributed by protohaem IX. Single crystals of bacterioferritin of the space group I432 suggest that the molecule is made up of 24 identical subunits related by a cubic point symmetry. The molecular weight of the protein subunit, as determined by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis, is 15000. In the electron microscope the bacterioferritin molecule appears to be a sphere of 9.5 nm (95 A) diameter composed of a negatively staining outer shell and an inner electron-dense core of 6 nm (60 A) diameter.

Apoproteins↗

Red cell ghost-entrapped deferoxamine as a model clinical targeted delivery system for iron chelators and other compounds.

In iron overload resulting from repeated blood transfusion, phagocytic reticuloendothelial cells are the primary and major sites of iron accumulation. Removal of this iron by the iron chelator deferoxamine can be enhanced by targeted delivery of this agent to reticuloendothelial cells. We have used resealed erythrocyte ghosts as a model system for delivery of deferoxamine to reticuloendothelial cells and have demonstrated a several-fold enhancement of urine iron excretion in children and adults with congenital or acquired iron-loading anemias. Although presently not cost-effective, this approach provides a useful, practical and safe model for [1] iron chelator targeting to reticuloendothelial cells, and [2] the clinical use of resealed erythrocyte ghosts for targeting pharmacologic agents to reticuloendothelial cells.

Deferoxamine↗

Iron-induced interleukin-6 gene expression: possible mediation through the extracellular signal-regulated kinase and p38 mitogen-activated protein kinase pathways.

Increased iron store in the body may increase the risk of many diseases such as cancer and inflammation. However, the precise pathogenic mechanism of iron has not yet been elucidated. In the present study, the early biological responses of cells to iron treatment were investigated in AP-1 luciferase reporter stably transfected mouse epidermal JB6 cells and primary rat hepatocytes. It was shown that water-soluble iron compounds, such as FeSO4 and Fe2(SO4)3, were more active in inducing AP-1 in JB6 cells than water-insoluble iron compounds, such as Fe2O3 and FeS. Iron stimulated mitogen-activated protein kinase (MAPK) family members of extracellular signal-regulated kinases (ERKs) and p38 MAPK but not c-jun NH2 terminal kinases (JNKs), both in JB6 cells and in primary rat hepatocytes, as determined by the phosphorylation assay. Interestingly, the increase in AP-1 luciferase activity by iron was inhibited by the pretreatment of the cells with PD98059, a specific MEK1 inhibitor, and SB202190, a p38 kinase inhibitor. Levels of interleukin-6 (IL-6), a pro-inflammatory cytokine, were increased in JB6 cells by iron in a dose-dependent manner. The increase in IL-6 and its mRNA by iron was also eliminated by the pretreatment of the cells with PD98059 and SB202190. Since the IL-6 promoter contains an AP-1 binding site, our studies indicate that the iron-induced IL-6 gene expression may be mediated through ERKs and p38 MAPK pathways, possibly one of the important mechanisms for the pathogenesis of iron overload.

Animals↗

In vitro activity of iron-binding compounds against Senegalese isolates of Plasmodium falciparum.

OBJECTIVES: The in vitro activities of FR160, a synthetic catecholate siderophore, and two iron-binding agents, desferrioxamine and doxycycline, were evaluated against Plasmodium falciparum isolates. Correlations between these compounds and standard antimalarial drugs (chloroquine, quinine, amodiaquine, pyronaridine, artemether, artesunate, atovaquone, cycloguanil and pyrimethamine) were assessed to determine any degree of cross-resistance. METHODS: Between October 1997 and February 1998, and September and November 1998, 189 P. falciparum isolates were obtained in Dielmo and Ndiop (Dakar). Their susceptibilities were assessed using an isotopic, microwell format, drug susceptibility test. RESULTS: The 137 inhibitory concentrations (IC(50)) values of FR160 ranged from 0.1 to 10 microM and the geometric mean IC(50) was 1.48 microM (95% CI = 1.29-1.68 microM). The geometric mean IC(50) of doxycycline for 121 isolates was 18.9 microM (95% CI = 16.8-21.3 microM) and that of desferrioxamine for 73 isolates was 20.7 microM (95% CI = 17.3-24.8 microM). FR160 was significantly less active against the chloroquine-resistant isolates (P < 0.0001). The mean IC(50)s of doxycycline were significantly higher for the chloroquine-susceptible isolates than for the resistant parasites (P = 0.0447). There was a weak correlation between the responses to FR160, desferrioxamine or doxycycline and those to the other antimalarial compounds (r(2) < 0.22). CONCLUSIONS: The activities of FR160 and desferrioxamine, determined for P. falciparum clones, were confirmed against 137 isolates. The coefficients of determination between the responses to FR160, doxycycline or desferrioxamine and those to all the antimalarial drugs tested are too weak to suggest cross-resistance. FR160 could be a rationale partner to use in combination with doxycycline.

Animals↗

Transferrins and heme-compounds as iron sources for pathogenic bacteria.

The low concentration of free iron in body fluids creates bacteriostatic conditions for many microorganisms and is therefore an important defense factor of the body against invading bacteria. Pathogenic bacteria have developed several mechanisms for acquiring iron from the host. Siderophore-mediated iron uptake involves the synthesis of low molecular weight iron chelators called siderophores which compete with the host iron-binding glycoproteins lactoferrin (LF) and transferrin (TF) for iron. Other ways to induce iron uptake, without the mediation of siderophores, are the possession of outer membrane protein receptors that actually recognize the complex of TF or LF with iron, resulting in the internalization of this metal, and the use of heme-compounds released into the circulation after lysis of erythrocytes. In this review, the nonsiderophore-mediated iron-uptake systems used by certain pathogenic bacteria are emphasized. The possible contribution of these iron-uptake systems to the virulence of pathogens is also discussed.

Bacteria↗

Roles of bioavailable iron and calcium in coal dust-induced oxidative stress: possible implications in coal workers' lung disease.

Marked regional differences in prevalence of pneumoconiosis are apparent in the US despite comparable dust exposure. In the present study, we examined the ability of 28 coal samples to release bioavailable iron (BAI) and calcium, as well as other metals such as Cr, Ni, Cu, and Co, from three coal mine regions in Utah (UT), West Virginia (WV), and Pennsylvania (PA), respectively. BAI is defined as iron (both Fe2+ and Fe3+) released by the coals in 10 mM phosphate solution, pH 4.5, which mimics conditions of the phagolysosomes in cells. We found that coals from the UT, WV, and PA regions released average levels of BAI of 9.6, 4658.8, and 12149 parts per million (ppm, w/w), respectively, which correlated well with the prevalence of pneumoconiosis from that region (correlation coefficient r = 0.92). The low levels of BAI in the UT coals were due to the presence of calcite (CaCO3), which was shown to be preferentially acid solubilized before iron compounds. Release of iron by two coal samples from the PA and UT regions was further examined in vitro in human lung epithelial A549 cells. We found that the coal from PA, with a high prevalence of pneumoconiosis, released BAI in a dose-dependent manner, both in tissue culture media and in A549 cells. At 2 microg/cm2, levels of lipid peroxidation induced by the PA coal were increased 112% over control cells at 24 h treatment, and were sustained at this level for 3 days. The coal from UT, with a low prevalence of pneumoconiosis, induced a marginal increase in cellular iron at 5 and 10 microg/cm2 treatments and had no effect on lipid peroxidation. Calcium levels in the cells treated with the PA and UT coals were 8.6 and 11.5 micromoles/10(6) cells, respectively, and were significantly higher than that in the controls (5.3 micromoles/10(6) cells) [corrected]. Our results suggest that the differences in the BAI content in the coals may be responsible for the observed regional differences in the prevalence of pneumoconiosis. Therefore, BAI may be a useful characteristic of coal for predicting coal's toxicity.

Biological Availability↗

Sodium iron EDTA [NaFe(III)EDTA] as a food fortificant: erythrocyte incorporation of iron and apparent absorption of zinc, copper, calcium, and magnesium from a complementary food based on wheat and soy in healthy infants.

BACKGROUND: Phytic acid is a strong inhibitor of iron absorption from fortified foods. In adults, this inhibitory effect can be overcome by adding ascorbic acid with the iron fortificant or by using a "protected" iron compound such as NaFeEDTA. In addition, the use of NaFeEDTA as an iron fortificant has been reported to increase zinc absorption in adult women. No information is available on iron bioavailability from NaFeEDTA or the influence of NaFeEDTA on minerals and trace elements in infants. OBJECTIVE: We aimed to compare iron bioavailability from a complementary food based on wheat and soy fortified with either NaFeEDTA or ferrous sulfate plus ascorbic acid. The apparent absorption of zinc, copper, calcium, and magnesium was evaluated in parallel. DESIGN: Stable-isotope techniques were used in a crossover design to evaluate erythrocyte incorporation of iron 14 d after administration of labeled test meals and the apparent absorption of zinc, copper, calcium, and magnesium on the basis of fecal monitoring in 11 infants. RESULTS: Geometric mean erythrocyte incorporation of iron was 3.7% (NaFeEDTA) and 4.9% (ferrous sulfate plus ascorbic acid) (P = 0.08). No significant differences in the apparent absorption of zinc, copper, calcium, or magnesium were observed between test meals (n = 10). CONCLUSIONS: Iron bioavailability from a high-phytate, cereal-based complementary food fortified with either NaFeEDTA or ferrous sulfate plus ascorbic acid was not significantly different. NaFeEDTA did not influence the apparent absorption of zinc, copper, calcium, or magnesium. NaFeEDTA does not provide any nutritional benefit compared with the combination of a highly bioavailable iron compound and ascorbic acid.

Biological Availability↗

[The effect of thiol compounds and iron on formation of nitric oxide from nitroprusside and nitroglycerin].

Some thiol-containing substances 5-Na-thiosulfate, cysteine, reduced glutathione and reducing agent Na-dethionite were shown to elevate formation of nitric oxide from both Na-nitroprusside and nitroglycerol in water solutions, especially if Fe2+ was added into solution of nitroglycerol. Nitric oxide developed was maintained in solutions in the complexes containing water soluble dinitrosyl iron and thiol derivatives. Release of nitric oxide from nitroprusside and nitroglycerol in animals was caused by similar reactions. At the same time, nitric oxide, derived from nitroprusside, was involved in complexes containing dinitrosyl iron and a protein with double thiol group, whereas nitric oxide, obtained from nitroglycerol, was bound with hemoglobin, producing Hb-nitrosyl complexes.

Chemical Phenomena↗

Determination of the iron state in ferrous iron containing vitamins and dietary supplements: application of Mössbauer spectroscopy.

Determination of the iron state in commercially manufactured iron containing vitamins and dietary supplements is important for evaluation of pharmaceuticals quality. Mössbauer (nuclear gamma-resonance) spectroscopy was used for analyzing the iron state in commercial pharmaceutical products containing ferrous fumarate (FeC(4)H(2)O(4)), ferrous sulfate (FeSO(4)), ferrous bisglycinate chelate (Ferrochel) and ferrous iron (hydrolyzed protein chelate). Mössbauer parameters and the iron states were determined for iron compounds in the studied pharmaceuticals. Various ferric and ferrous impurities were found in all of the commercial products. The quantities of ferric impurities exceeded the FDA limitation of 2% in products containing ferrous fumarate. The quantities of ferric impurities exceeded 58% and 30% in products containing ferrous bisglycinate chelate and ferrous iron (hydrolyzed protein chelate), respectively. The presence of ferrous and ferric impurities was not related to the ageing of the vitamins and dietary supplements. Two pharmaceutical products contained major iron compounds, the Mössbauer parameters of which did not correspond to the ferrous fumarate or ferrous bisglycinate chelate claimed by the manufacturer.

Dietary Supplements↗

Preliminary observation of elevated levels of nanocrystalline iron oxide in the basal ganglia of neuroferritinopathy patients.

Magnetometry analysis of brain tissue sub-samples from two neuroferritinopathy patients provides a preliminary indication that the amount of magnetic iron compounds associated with this rare disease is significantly larger than in age/sex-matched controls. The primary iron compounds contributing to the remnant magnetization of the tissue above 50 K and at body temperature are both blocked and superparamagnetic (SPM) biogenic magnetite (Fe3O4) and/or maghemite (gamma-Fe2O3). The concentration of SPM magnetite is significant and appears to be proportional to the concentration of ferritin, which varies with progression of the disease. The mutated ferritin protein appears to be responsible for the presence of iron oxide nano-particules, which in turn could be responsible for extensive damage in the brain.

Aged↗