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PubMed2002

Phosphorus fractionation in lake sediments--lakes Volvi and Koronia, N. Greece.

Sediments from two lakes, the meso-to-eutrophic Volvi and the hypertrophic Koronia, located in N. Greece were examined on the basis of P-fractionation. In both lakes, the rank order of P-fractions was HCl-P > NaOH-P > BD-P > NH4Cl-P. The loosely sorbed phosphorus (NH4Cl-P) represented < 1% of the sedimentary inorganic phosphorus, while the reductant phosphorus (BD-P) ranged 5-6%. The calcium bound phosphorus (HCl-P) showed considerable contribution (59-74%) to the sedimentary inorganic P-loads. The metal oxide bound phosphorus (NaOH-P) was higher in the hypertrophic (30-35%) than in the meso-to-eutrophic system (19-28%). Fine-sized sediments exhibited significantly higher concentrations of HCl-P in Volvi and NH4Cl-P in Koronia. Sampling month had significant effect in variance of most P-fractions and other sediment features in both lakes. Use was also made of multivariate statistics to identify the factors which influence the sedimentary phosphorus. NaOH-P was the most reactive fraction in Lake Volvi. Iron compounds and organic matter seem to play a significant role in regulating this labile P-budget. NH4Cl-P was the more reactive fraction in Lake Koronia which was influenced by sedimentation of P-absorbed on clay/silt fine particles.

Calcium↗
PubMed2004

Reduction of aqueous chromate by Fe(II)/Fe(III) carbonate green rust: kinetic and mechanistic studies.

This work describes the heterogeneous reaction between FeII in carbonate green rust and aqueous chromate, in NaHCO3 solutions at 25 degrees C, and at pH values of 9.3-9.6. Evidence for reduction of CrVI to CrIII and concomitant solid-state oxidation of lattice FeII to FeIII was found from FeII titration and from structural analysis of the solids using FTIR, XRD, SEM, and XPS methods. Results indicate the formation of ferric oxyhydroxycarbonate and the concomitant precipitation of CrIII monolayers at the surface of the iron compound that induce passivation effects and progressive rate limitations. The number of CrIII monolayers formed at the completion of the reaction depends on [FeII]t=0, the molar concentration of FeII(solid) at t=0; on [n(o)]t=0, the molar concentration of reaction sites present at the surface of the solid phase at t=0; and on [CrVI]t=0, the molar concentration of CrVI at t=0. Kinetic data were modeled using a model based on the formation of successive CrIII monolayers, -(d[CrVI]/dt) = sigma(1)j k(i)[S] [CrVI]([n(i - 1)] - [n(i)]) with k(i)[S] (in s(-1) L mol(-1)), the rate coefficient of formation of CrIII monolayer i, and [n(i)] and [n(i - 1)], the molar concentration of CrIII precipitated in monolayer i and monolayer i - 1, respectively. Good matching curves were obtained with kinetic coefficients: k(1)[S] = 5-8 x 10(-4), k(2)[S] = 0.5-3 x 10(-5), and k(3)[S] about 1.7 x 10(-6) s(-1) m(-2) L. The CrVI removal efficiency progressively decreases along with the accumulation of CrIII monolayers at the surface of carbonate green rust particles. In the case of thick green rust particles resulting from the corrosion of iron in permeable reactive barriers, the quantity of FeII readily accessible for efficient CrVI removal should be rather low.

Carbonates↗
PubMed1997

Effect of haemin on the enterotoxin production of Campylobacter jejuni.

When Campylobacter jejuni was exposed to iron compounds, alterations in enterotoxin production were monitored by enzyme linked immunosorbent assay (ELISA) and Western blotting. By ELISA, treatment with 10 microM haemin increased the ganglioside binding activity of the toxin in the extracellular fraction but not in the intracellular fraction. By Western blotting, a 68 kD subunit of the enterotoxin was observed to increase in concentration. The results suggest that haemin may have a positive regulation effect on enterotoxin maturation when released from bacterial cells.

Animals↗
PubMed2005

Recovery from iron deficiency in rats by the intake of recombinant yeast producing human H-ferritin.

OBJECTIVE: This study examined whether iron accumulated in ferritin-producing recombinant microbes is bioavailable to rats with iron deficiency. METHODS: Rats induced with iron deficiency were treated with iron preparations of ferrous ammonium sulfate, horse spleen ferritin, control yeast, and ferritin-producing recombinant yeast for 14 d. The bioavailability of iron was examined by measuring hemoglobin concentration, hematocrit value, and tissue iron stores. Differences between dietary groups were determined by one-way analysis of variance, and P < 0.05 was considered statistically significant. RESULTS: Based on hemoglobin concentration and hematocrit value, iron in ferrous ammonium sulfate, horse spleen ferritin, and ferritin-producing yeast were bioavailable to rats and cured iron deficiency. The efficacy of ferritin and ferritin-producing yeast was also confirmed in establishing tissue iron stores after induction of iron deficiency. CONCLUSIONS: The iron sources of ferritin and ferritin-producing yeast were as effective in recovery from iron deficiency as the iron compounds of ferric citrate and ferrous ammonium sulfate. The results suggest that the iron stored in the ferritin of recombinant yeast is bioavailable, and that recombinant yeast may contribute widely as a source of iron to resolve the global problem of iron deficiency.

Analysis of Variance↗
PubMed2006

Chloroquine inhibits Paracoccidioides brasiliensis survival within human monocytes by limiting the availability of intracellular iron.

The mechanisms used by Paracoccidioides brasiliensis(Pb 18) to survive into monocytes are not clear. Cellular iron metabolism is of critical importance to the growth of several intracellular pathogens, including P. brasiliensis, whose capacity to multiply in mononuclear phagocytes is dependent on the availability of intracellular iron. Chloroquine, by virtue of its basic properties, has been shown to prevent release of iron from holotransferrin by raising endocytic and lysosomal pH, and thereby interfering with normal iron metabolism. Then, in view of this, we have studied the effects of CHLOR on P. brasiliensis multiplication in human monocytes and its effect on the murine paracoccidioidomycosis. CHLOR induced human monocytes to kill P. brasiliensis. The effect of CHLOR was reversed by FeNTA, an iron compound that is soluble at neutral to alkaline pH, but not by holotransferrin, which releases iron only in an acidic environment. CHLOR treatment of Pb 18-infected BALB/c mice significantly reduced the viable fungi recovery from lungs, during three different periods of evaluation, in a dose-dependent manner. This study demonstrates that iron is of critical importance to the survival of P. brasiliensis yeasts within human monocytes and the CHLOR treatment in vitro induces Pb 18 yeast-killing by monocytes by restricting the availability of intracellular iron. Besides, the CHLOR treatment in vivo significantly reduces the number of organisms in the lungs of Pb-infected mice protecting them from several infections. Thus, CHLOR was effective in the treatment of murine paracoccidioidomycosis, suggesting the potential use of this drug in patients' treatment.

Animals↗
PubMed1991

The relative efficiency of radicals in radiation damage to deoxyribose.

The radiation damage to Deoxyribose was studied with a view to identify the damaging species. Our results indicate that H, eaq-, CO2- do not cause any appreciable damage in the absence of metal compounds and .OH is the sole damaging entity. Iron compounds sensitize very little O2- damage and CO2- damage could not be sensitized. In N2-saturated solutions metal compounds increase the damage by converting eaq- into deleterious .OH.

Copper↗
PubMed1993

Ferrous sulfate reduces cimetidine absorption.

A variety of drugs that bind to iron have significant reductions in absorption when coadministered with iron compounds. Cimetidine has a structure that would suggest strong binding to iron ions. In vitro experiments were performed to examine a variety of characteristics of the binding of iron to cimetidine. Further studies were conducted to determine the effect of concurrent administration of ferrous sulfate on cimetidine absorption in an in vivo isolated perfused rat jejunal model of drug absorption. The dose of cimetidine was chosen to represent a human dose of 300 mg, while the ferrous sulfate doses were chosen to represent 150- and 300-mg doses. The higher ferrous sulfate dose completely inhibited cimetidine absorption (P < 0.01), while the lower dose of ferrous sulfate caused a 63% reduction in cimetidine absorption (P < 0.05). In vitro iron in its ferrous from rapidly oxidizes to the ferric form. The ferric form of iron binds to cimetidine and may be the cause of the decreased cimetidine absorption. Care should be taken in prescribing iron supplements with cimetidine.

Animals↗
PubMed1998

Accumulation of iron by primary rat hepatocytes in long-term culture: changes in nuclear shape mediated by non-transferrin-bound forms of iron.

We have previously shown that hepatocytes in long-term dimethylsulfoxide (DMSO) culture, fed a chemically defined medium, are highly differentiated and an excellent in vitro model of adult liver. Hepatocytes in long-term DMSO culture can be iron loaded by exposure to non-transferrin-bound iron (NTBI) in the form of ferrous sulfate (FeSO4), ferric nitrilotriacetate, or trimethylhexanoyl (TMH)-ferrocene. Holotransferrin, at equivalent times and concentrations, was unable to load hepatocytes. Of the iron compounds tested, TMH-ferrocene most accurately simulated the morphological features of iron-loaded hepatocytes in vivo. When exposed to 25 micromol/L TMH-ferrocene, hepatocytes loaded increasing amounts of iron for 2 months before the cells died. When exposed to lower concentrations of TMH-ferrocene (as low as 2.5 micromol/L), hepatocytes continuously loaded iron and remained viable for more than 2 months. The cellular deposition of iron was different in hepatocytes exposed to TMH-ferrocene compared with those exposed to FeSO4; exposure to TMH-ferrocene resulted in the presence of more ferritin cores within lysosomes than were seen with FeSO4. When the concentration of TMH-ferrocene was increased, a greater number of ferritin cores were observed within the lysosome, and total cellular ferritin, as assessed by Western blot, increased. The formation of hemosiderin was also observed. Furthermore, nuclear shape was distorted in iron-loaded hepatocytes. The extent of deviation from circularity in the nucleus correlated with increasing concentrations of TMH-ferrocene and was greater in hepatocytes exposed to FeSO4 than an equivalent concentration of TMH-ferrocene. The deviation from circularity was smallest in hepatocytes that contained well formed ferritin cores and increased in hepatocytes that contained greater amounts of hemosiderin. Furthermore, in hepatocytes treated with FeSO4, a large amount of cell-associated iron was detected but without a significant increase in the total amount of ferritin. The deviation from circularity was the largest in FeSO4-treated hepatocytes, indicating that iron not properly incorporated into ferritin caused more cellular damage. We conclude that iron-loaded hepatocytes in long-term DMSO culture represent a flexible system for studying the effects of chronic iron loading on hepatocytes.

Animals↗
PubMed2004

57Fe NMR spectroscopy of ferrocenes bearing pi-acceptor substituents.

Ferrocene derivatives bearing pi-acceptor substituents in 1- or 1,1'-positions such as carbonyl group(s) (1, 2), a sulfinyl group (4) or boryl group(s) (5, 6, 9) and related [3]ferrocenophanes (3, 7, 10, 12, 13) and a [4]ferrocenophane (8) were studied by 57Fe NMR spectroscopy. The deshielding effect of the respective pi-acceptor substituent can be partially or fully compensated by distortion of the ferrocene geometry. Both aspects become apparent by comparing delta57Fe data of the [n]ferrocenophanes with those of related non-cyclic derivatives.

Ferrous Compounds↗
PubMed2002

Molecular and cellular mechanisms of iron homeostasis and toxicity in mammalian cells.

Iron is an essential metal for almost all living organisms due to its involvement in a large number of iron-containing enzymes and proteins, yet it is also toxic. The mechanisms involved in iron absorption across the intestinal tract, its transport in serum and delivery to cells and iron storage within cells is briefly reviewed. Current views on cellular iron homeostasis involving the iron regulatory proteins IRP1 and IRP2 and their interactions with the iron regulatory elements, affecting either mRNA translation (ferritin and erythroid cell delta-aminolaevulinate synthase) or mRNA stability (transferrin receptor) are discussed. The potential of Fe(II) to catalyse hydroxyl radical formation via the Fenton reaction means that iron is potentially toxic. The toxicity of iron in specific tissues and cell types (liver, macrophages and brain) is illustrated by studies with appropriate cellular and animal models. In liver, the high levels of cyoprotective enzymes and antioxidants, means that to observe toxic effects substantial levels of iron loading are required. In reticuloendothelial cells, such as macrophages, relatively small increases in cellular iron (2-3-fold) can affect cellular signalling, as measured by NO production and activation of the nuclear transcription factor NF kappa B, as well as cellular function, as measured by the capacity of the cells to produce reactive oxygen species when stimulated. The situation in brain, where anti-oxidative defences are relatively low, is highly regionally specific, where iron accumulation in specific brain regions is associated with a number of neurodegenerative diseases. In the brains of animals treated with either trimethylhexanoylferrocene or aluminium gluconate, iron and aluminium accumulate, respectively. With the latter compound, iron also increases, which may reflect an effect of aluminium on the IRP2 protein. Chelation therapy can reduce brain aluminium levels significantly, while iron can also be removed, but with greater difficulty. The prospects for chelation therapy in the treatment and possible prevention of neurodegenerative diseases is reviewed.

Animals↗
PubMed1969

Lipid peroxide formation in microsomes. The role of non-haem iron.

1. Metal ion-chelating agents such as EDTA, o-phenanthroline or desferrioxamine inhibit lipid peroxide formation when rat liver microsomes prepared from homogenates made in pure sucrose are incubated with ascorbate or NADPH. 2. Microsomes treated with metal ion-chelating agents do not form peroxide on incubation unless inorganic iron (Fe(2+) or Fe(3+)) in a low concentration is added subsequently. No other metal ion can replace inorganic iron adequately. 3. Microsomes prepared from sucrose homogenates containing EDTA (1mm) do not form lipid peroxide on incubation with ascorbate or NADPH unless Fe(2+) is added. Washing the microsomes with sucrose after preparation restores most of the capacity to form lipid peroxide. 4. Lipid peroxide formation in microsomes prepared from sucrose is stimulated to a small extent by inorganic iron but to a greater extent if adenine nucleotides, containing iron compounds as a contaminant, are added. 5. The iron contained in normal microsome preparations exists in haem and in non-haem forms. One non-haem component in which the iron may be linked to phosphate is considered to be essential for both the ascorbate system and NADPH system that catalyse lipid peroxidation in microsomes.

Animals↗
PubMed1988

Iron toxicity in neonatal foals.

Newborn Shetland foals died of acute hepatic failure following oral administration of approximately 16 mg/kg body weight ferrous fumarate. Lesions in these foals were indistinguishable from lesions in foals given an oral digestive inoculant containing ferrous fumarate and were also similar to the syndrome characterised as 'toxic hepatopathy' in foals in the United States in 1983. We conclude that foals are susceptible to toxicity from low doses of iron compounds in the first few days of life. Vitamin E and selenium deficiency may contribute to this susceptibility.

Administration, Oral↗
PubMed1980

Distribution of iron in sphaerotilus and the associated inhibition.

The distribution of iron between the sheaths and the cells of iron-inhibited Sphaerotilus cultures was determined. The experiment was conducted with different soluble iron forms as inhibitors. The growth inhibition was found to be related to the iron sorbed by the cells rather than by the sheaths. At the 90% inhibition level, iron sorbed by the cells ranged from 13 to 15 mg/g of organism for all three inhibitors tested. For 50% inhibition, the iron sorbed by the cells ranged from 7 to 8 mg/g of organism. The iron sorbed by the sheaths varied widely, ranging from 23 to 118 mg/g of organism at the 90% inhibition level and from 11 to 61 mg/g at the 50% inhibition level. The degree of inhibition is closely related to the amount of iron sorbed by the cells, which in turn is a function of the type of iron compound or complex used. The solubility of the iron is a major consideration.

Journal Article↗