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PubMed1992

Iron modulates interferon-gamma effects in the human myelomonocytic cell line THP-1.

This investigation demonstrates that low concentrations (25 microM) of free and transferrin-bound iron reduce the efficiency of the interferon-gamma (IFN-gamma) signal in the human myelomonocytic cell line THP-1, as seen by decreased production of neopterin, reduced degradation of tryptophan, and impaired expression of major histocompatibility complex (MHC) class II antigens. This inhibitory effect of iron, which is not due to an enhanced cytotoxicity towards THP-1 cells, is increased by enhancement of iron concentrations in a dose-dependent relationship and can be partially reversed by increasing amounts of the cytokine. The iron-mediated inhibition of the effects of IFN-gamma is fully reversed when iron is administered concomitantly with equimolar concentrations of the iron chelator deferoxamine. Furthermore, deferoxamine alone is even able to enhance the efficiency of the IFN-gamma signal. Our data provide evidence that there is an inverse correlation between the intracellular amount of iron, which is not bound to ferritin, and the activity of the IFN-gamma signal. This suggests that iron withholding by the immune cells in the course of inflammatory disorders may also contribute to the enhancement of the cytopathic effect of IFN-gamma. This speculation is confirmed by the observation of high concentrations of immune activation markers such as IFN-gamma and neopterin and low serum iron levels in patients with hypoferric anemia in the course of chronic inflammation.

Biopterins↗

PubMed1992

Effects of vitamin E on the killing of cultured hepatocytes by tert-butyl hydroperoxide.

The disposition of vitamin E was examined in cultured rat hepatocytes intoxicated with tert-butyl hydroperoxide (TBHP). Culturing of the cells overnight (18-20 hr) with approximately 60 nM alpha-tocopherol (alpha-T) equivalents [Williams' E medium, 18 nM tocopherol phosphate (alpha-TP), 9% fetal calf serum, 43 nM alpha-T] resulted in a content of alpha-T that was 16% of the concentration of vitamin E measured in freshly isolated hepatocytes. Supplementation of the medium with 1 microM alpha-TP maintained the alpha-T concentration of the cultured cells at the level of freshly isolated hepatocytes. Supplemented hepatocytes exposed to TBHP showed decreased lipid peroxidation and delayed cell killing, compared with hepatocytes not cultured overnight with alpha-TP. Killing of the supplemented cells by TBHP was accompanied by a loss of alpha-T. Pretreatment of supplemented hepatocytes with the iron chelator deferoxamine prevented much of the loss of alpha-T. At the same time, deferoxamine inhibited both the lipid peroxidation and cell killing. The antioxidant N,N'-diphenyl-1,4-phenylenediamine reduced the loss of alpha-T and significantly decreased lipid peroxidation. In the presence of N,N'-diphenyl-1,4-phenylenediamine, cell killing was delayed by 15 min and reduced in extent. Overnight supplementation of hepatocytes with nonesterified alpha-T, or vitamin E esters other than alpha-TP, similarly rendered the cells less sensitive to TBHP. The nonesterified alpha-T produced a higher cell-associated vitamin E concentration than did the esters; however, nonesterified alpha-T did not result in greater protection against TBHP. These data indicate that the mechanisms of the cell killing by TBHP are the same in cultured hepatocytes that contain low or physiological concentrations of vitamin E.

Animals↗

PubMed2005

The source of endogenous carbon monoxide formation in human placental chorionic villi.

Carbon monoxide (CO) is proposed to play a role in placental vascular control, as the placenta produces and responds to CO. The mechanism by which CO is formed by the placenta is unclear but could be through heme oxygenase (HO) degradation of heme, lipid peroxidation, or both. Human placental cotyledons were perfused with Kreb s solution to remove blood. Chorionic villi segments were prepared for measurements of CO production in the absence/presence of an exogenous supply of heme substrate (methemalbumin), inhibitors of HO, or inhibitors of lipid peroxidation. HO inhibitors used were chromium mesoporphyrin (CrMP) (0.1 mM, 0.3 mM), and azalanstat (0.1 mM, 0.3 mM). The lipid peroxidation inhibitors used were EDTA (0.1 mM, 0.3 mM) and deferoxamine (0.1 mM). Incubation of villi segments with methemalbumin (0.15 mM, 0.3 mM, 0.45 mM) resulted in a concentration-dependent increase in CO formation above the basal, endogenous rate. CrMP and azalanstat inhibited basal endogenous CO production, whereas EDTA and deferoxamine enhanced CO formation above basal level. These results demonstrate that endogenous CO was formed by human chorionic villi from heme, primarily through the action of HO, and are consistent with the hypothesis that HO plays a role in the regulation of placental vasculature by the formation of heme-derived CO.

Carbon Monoxide↗

PubMed1990

Iron loading of endothelial cells augments oxidant damage.

Transition metals, particularly iron, will potentiate oxidant damage to isolated cell organelles, plasma membranes, and DNA when added to in vitro incubation systems. However, similar studies of intact cells have been hampered by the relative impermeability of whole cells to iron. We have iron loaded cultured endothelial cells by using the iron-chelating fungistat 8-hydroxyquinoline (8HQ). 8HQ forms lipophilic chelates with iron and rapidly transfers the metal across the intact plasma membrane of endothelial cells. After brief exposure to 8HQ and subsequent thorough washing of endothelial cells, the cell-associated iron cannot be removed by the powerful chelator deferoxamine, clearly indicating the intracellular location of 8HQ-transported iron. Iron-loaded cells (but not cells exposed to high concentrations of 8HQ or iron separately) are extremely sensitive to oxidants (1) produced externally by phorbol-stimulated granulocytes, (2) generated intracellularly by menadione, or (3) added as H2O2. In the latter instance, as little as 7 mumol/L H2O2 provokes destruction of approximately 50% of iron-loaded endothelial cells, whereas untreated endothelium readily survives exposure to H2O2 concentrations as high as 2 mmol/L. Cytotoxicity is accompanied by membrane lipid peroxidation (formation of thiobarbituric acid-reactive substances). Both cytotoxicity and lipid peroxidation are inhibited by the lipophilic 21-aminosteroid U74500A ("lazaroid") (50% inhibitory concentration = approximately 0.5 mumol/L), whereas deferoxamine (250 mumol/L) is ineffective (suggesting iron intercalation into hydrophobic domains of the cell). We conclude that this pharmacologic model for iron loading of intact cells may yield valuable insights into the pathogenic importance of intracellular iron in iron overload states, inflammation, and cellular injury.

Animals↗

PubMed1990

[Systematic blood transfusions in adult homozygote sickle-cell anemia. Study of 11 cases followed for 5 to 10 years].

Eleven patients (5 men and 6 women) with sickle-cell anaemia were treated with systematic repeated blood transfusions to avoid the sickling crises and complications of the disease and were followed up for 5 to 10 years. On average, the patients received 22 erythrocyte concentrates per year, to a mean individual total of 180 sediments. Each blood transfusion was accompanied by an intravenous infusion of deferoxamine 2 grams. Systematic blood perfusions unquestionably had beneficial effects on the frequency of sickling crises and complications, as well as on the patients' quality of life and psycho-social status. On the other hand, the iron overload could not be avoided, and it sometimes resulted in haematochromatosis (2 patients). At the moment, only continuous deferoxamine infusions could prevent this from happening and enable blood transfusions to be more widely used, provided its indications, restricted to the most severe forms of the disease, are carefully weighed. In this series of patients, the risk of viral contamination seemed to be relatively low, and in particular no HIV seroconversion was detected.

Adolescent↗

PubMed1990

Kinetic studies on spin trapping of superoxide and hydroxyl radicals generated in NADPH-cytochrome P-450 reductase-paraquat systems. Effect of iron chelates.

Electron spin resonance (ESR) studies on spin trapping of superoxide and hydroxyl radicals by 5,5-dimethyl-1-pyrroline-1-oxide (DMPO) were performed in NADPH-cytochrome P-450 reductase-paraquat systems at pH 7.4. Spin adduct concentrations were determined by comparing ESR spectra of the adducts with the ESR spectrum of a stable radical solution. Kinetic analysis in the presence of 100 microM desferrioxamine B (deferoxamine) showed that: 1) the oxidation of 1 mol of NADPH produces 2 mol of superoxide ions, all of which can be trapped by DMPO when extrapolated to infinite concentration; 2) the rate constant for the reaction of superoxide with DMPO was 1.2 M-1 s-1; 3) the superoxide spin adduct of DMPO (DMPO-OOH) decays with a half-life of 66 s and the maximum level of DMPO-OOH formed can be calculated by a simple steady state equation; and 4) 2.8% or less of the DMPO-OOH decay occurs through a reaction producing hydroxyl radicals. In the presence of 100 microM EDTA, 5 microM Fe(III) ions nearly completely inhibited the formation of the hydroxyl radical adduct of DMPO (DMPO-OH) as well as the formation of DMPO-OOH and, when 100 microM hydrogen peroxide was present, produced DMPO-OH exclusively. Fe(III)-EDTA is reduced by superoxide and the competition of superoxide and hydrogen peroxide in the reaction with Fe(II)-EDTA seems to be reflected in the amounts of DMPO-OOH and DMPO-OH detected. These effects of EDTA can be explained from known kinetic data including a rate constant of 6 x 10(4) M-1 s-1 for reduction of DMPO-OOH by Fe(II)-EDTA. The effect of diethylenetriamine pentaacetic acid (DETAPAC) on the formation of DMPO-OOH and DMPO-OH was between deferoxamine and EDTA, and about the same as that of endogenous chelator (phosphate).

Animals↗

PubMed1990

A reexamination of the cytochrome P-450-catalyzed free radical production from a dihydropyridine. Evidence of trace transition metal catalysis.

Radical production from 3,5-bis(ethoxycarbonyl)-4-ethyl-2,6-dimethyl-1,4- dihydropyridine (DDEP) in rat liver microsomes has been attributed to one-electron oxidation via cytochrome P-450 followed by extrusion of an ethyl radical. In the presence of the spin trap alpha-(4-pyridyl 1-oxide)-N-tert-butylnitrone (4-POBN), this radical was detected as the 4-POBN/ethyl radical adduct by electron paramagnetic resonance spectroscopy. The addition of catalase resulted in over a 50% decrease in radical production. The concentration of the 4-POBN/ethyl radical adduct increased about 9-fold in the presence of EDTA and approximately 2-fold in the presence of either diethylenetriaminepentaacetic acid (DTPA) or deferoxamine mesylate. When DDEP was incubated with deferoxamine mesylate-washed microsomes and NADPH in Chelex-treated incubation buffer, much less 4-POBN/ethyl radical formation occurred. Addition of either DTPA, EDTA, or the ferric complexes of these chelators greatly stimulated production of the 4-POBN/ethyl radical adduct in this system. These results suggest that the ethyl radicals produced from DDEP in a microsomal system arise via trace transition metal-catalyzed reactions.

Animals↗

PubMed1990

Methodological issues in studying the effect of the new oral chelator 1,2-dimethyl-3-hydroxypyrid-4-one (L1) on absorption of iron.

Although deferoxamine is currently the drug of choice for iron chelation, there is more and more evidence of its toxicity. As a replacement for deferoxamine, 1,2-dimethyl-3-hydroxypyrid-4-one (L1), a new oral iron chelator, is undergoing clinical studies in thalassemic patients. Iron handling in experimental acute iron intoxication is being studied in a multiphase study. Preliminary results suggest that the L1-iron complex is not absorbed from the gastrointestinal tract. Methodological issues in studying iron chelation in the context of acute iron intoxication are presented.

Administration, Oral↗

PubMedDate not supplied

Aluminum in parenteral products: medical perspective on large and small volume parenterals.

Bone abnormalities may complicate parenteral nutrition (PN) therapy given to patients. Bone disease, manifested by reduced bone formation and demineralization in adults, and poor mineralization in infants, is associated with bone aluminum accumulation at the mineralizing surface. Aluminum was first shown to contaminate casein hydrolysate, the PN protein source. Substitution of amino acid solutions, low in aluminum, reduced bone aluminum and improved bone formation in adults. Aluminum also accumulates ten-fold in the bones of premature infants receiving chronic PN. Present sources of aluminum in PN are calcium and phosphate salts, albumin, and heparin. Although increased bone aluminum in infants is not proven to cause disease, use of deferoxamine in one infant produced hypocalcemia. This suggested that chelation of bone aluminum by deferoxamine increased bone calcium uptake. Thus aluminum in bone may impair bone calcium uptake and may contribute to the pathogenesis of PN-related bone disease in infants. Another complication of PN therapy in infants is cholestatic liver disease, manifested by reduced bile flow, and, occasionally, gallstones. Aluminum has been found to accumulate in the livers of these infants, and there is experimental evidence that aluminum can reduce bile flow both in rats and in piglets. Aluminum contamination of PN solutions puts infants at increased risk for complications of PN therapy; amounts of aluminum in PN solutions should therefore be minimized.

Adult↗

PubMed1989

Measurement and characterization of postischemic free radical generation in the isolated perfused heart.

Electron paramagnetic resonance spectroscopy has been applied to measure radical generation in the postischemic heart; however, there is controversy regarding the methods used and the conclusion as to whether radicals are generated. In order to resolve this controversy, direct and spin trapping measurements of the time course and mechanisms of radical generation were performed in isolated perfused rabbit hearts. In reperfused tissue, 3 prominent radical signals are observed: A, isotropic g = 2.004 suggestive of a semiquinone; B, anisotropic g parallel = 2.033 and g perpendicular = 2.005 suggestive of ROO.; and C, a triplet g = 2.000 and aN = 24 G suggestive of a nitrogen centered radical. B and C, however, are highly labile and disappear at temperatures probably encountered in some previous studies. In normally perfused hearts, A is observed with only small amounts of B and C. During ischemia, B and C increase reaching a maximum after 45 min while A decreases. On reflow with oxygenated perfusate all 3 signals increase. With varying duration of ischemia and reflow, peak signal intensities occurred after 15 s of reflow following 30 min of ischemia. Reperfusion with superoxide dismutase, deferoxamine, or mannitol abolished the reperfusion increase of B. Measurements performed with the spin trap 5,5'-dimethyl-1-pyrroline-N-oxide (DMPO) demonstrated a similar time course of radical generation with prominent DMPO-OH and DMPO-R signals peaking between 10 and 20 s of reflow. Superoxide dismutase and deferoxamine also quenched these signals. Thus, .O2- derived .OH, R., and ROO. radicals are generated in postischemic myocardium. While the experimental techniques used can result in loss of intrinsic radicals and generation of extraneous radicals, with proper care and controls valid measurements of free radicals in biological tissues can be performed.

Animals↗

PubMed1989

[Yersinia enterocolitica infections and thalassemia major in children].

We report two cases of severe Yersinia enterocolitica infection in children with homozygous thalassemia. One patient had septicemia and the other had mesenteric adenitis. Two factors can enhance the infectivity of Yersinia enterocolitica in children with thalassemia: iron overload and deferoxamine therapy. Laparotomy and cefotaxime-netilmicin therapy were successful in the patient with mesenteric adenitis. In the patient with septicemia, cefotaxime-netilmicin, then doxycycline-netilmicin failed, and recovery was finally achieved under rifampicin-netilmicin. Because of the possibility of septicemic dissemination secondary to digestive Yersinia enterocolitica infection in children with thalassemia, we advocate immediate discontinuation of deferoxamine and prescription of oral antimicrobial therapy (trimethoprim-sulfamethoxazole for instance) in every thalassemic patient with febrile diarrhea.

Adolescent↗

PubMed1985

Pulmonary endothelial cell killing by human neutrophils. Possible involvement of hydroxyl radical.

Human blood neutrophils stimulated by a variety of agents were shown to have cytotoxic effects on bovine pulmonary artery endothelial cells. Effective agonists included immune complexes, opsonized zymosan and 12-O-tetradecanoyl phorbol acetate. Unstimulated human neutrophils and neutrophils stimulated with N-formyl-methionyl-leucyl-phenylalanine or with platelet-activating factor failed to induce significant killing even though secretory release of lysosomal enzymes occurred. In comparing the effects of the different agonists, endothelial cell killing showed a better correlation with the production of H2O2 than with the generation of O2-. Endothelial cell killing by stimulated human neutrophils was inhibited by catalase but not by soybean trypsin inhibitor or superoxide dismutase. Killing was also inhibited by two scavengers (N, N-dimethylthiourea and D-mannitol) of hydroxyl radical and by deferoxamine mesylate, an iron-chelator. Iron-saturated deferoxamine mesylate was significantly less effective in protecting the endothelial cells against killing. Agents that were protective against endothelial cell killing did not interfere with the generation of O2- in stimulated neutrophils. These results suggest that leukocyte-induced endothelial cell killing in vitro can be induced by some but not all agonists for neutrophils and that the killing is oxygen-dependent and may be directly due to hydroxyl radical production.

Animals↗

PubMed1988

Nonheme iron in sickle erythrocyte membranes: association with phospholipids and potential role in lipid peroxidation.

Previous studies documented the abnormal association of heme and heme proteins with the sickle RBC membrane. We have now examined RBC ghosts and inside-out membranes (IOM) for the presence of nonheme iron as detected by its formation of a colored complex with ferrozine. Sickle ghosts have 33.8 +/- 18.2 nmol nonheme iron/mg membrane protein, and sickle IOM have 4.3 +/- 3.0 nmol/mg. In contrast, normal RBC ghosts and IOM have no detectable nonheme iron. The combination of heme and nonheme iron in sickle IOM averages nine times the amount of membrane-associated iron in normal IOM. Kinetics of the ferrozine reaction show that some of this nonheme iron on IOM reacts slowly and is probably in the form of ferritin, but most (72% +/- 18%) reacts rapidly and is in the form of some other biologic chelate. The latter iron compartment is removed by deferoxamine and by treatment of IOM with phospholipase D, which suggests that it represents an abnormal association of iron with polar head groups of aminophospholipids. The biologic feasibility of such a chelate was demonstrated by using an admixture of iron with model liposomes. Even in the presence of tenfold excess adenosine diphosphate, iron partitions readily into phosphatidylserine liposomes; there is no detectable association with phosphatidylcholine liposomes. To examine the bioavailability of membrane iron, we admixed membranes and t-butylhydroperoxide and found that sickle membranes show a tenfold greater peroxidation response than do normal membranes. This is not due simply to a deficiency of vitamin E, and this is profoundly inhibited by deferoxamine. Thus, while thiol oxidation in sickle membranes previously was shown to correlate with heme iron, the present data suggest that lipid peroxidation is related to nonheme iron. In control studies, we did not find this pathologic association of nonferritin, nonheme iron with IOM prepared from sickle trait, high-reticulocyte, postsplenectomy, or iron-overloaded individuals. These data provide additional support for the concept that iron decompartmentalization is a characteristic of sickle RBCs.

Adsorption↗

PubMed1987

Acute iron intoxication: treatment controversies.

Accidental ingestion of iron-containing preparations is a common, serious pediatric problem. Despite the frequency of this type of ingestion, the treatment remains under dispute. Controversies surrounding the use of sodium bicarbonate and phosphate solutions for complexation, oral deferoxamine lavage, and the deferoxamine provocation test are discussed. Therapeutic recommendations are made based on a review of the literature.

Chelating Agents↗

PubMed1978

Iron metabolism and its responses to allopurinol treatment in porphyria cutanea tarda.

Iron kinetics, absorption and storage were studied by means of 59Fe and deferoxamine (Desferal-Ciba) in eight patients with porphyria cutanea tarda at the time of clinical activity and after allopurinol treatment. At the time of clinical manifestations, a significant impairment of erythrocyte-iron turnover and of radio-iron utilization was demonstrable in a half of the patients and a significant increase in iron absorption and turnover in patients out of 8. The measurements of surface activity in vivo showed a significant increase in storage iron. This was confirmed by the excessive urinary excretion of deferoxamine-iron, attaining three- to four-fold figures of the normal values (251 +/- 85 mg). The increased absorption of iron coupled with an abnormal porphyrin metabolism is suggestive of a double genetic defect. As a result of allopurinol treatment, normalization of iron kinetics and a moderate decrease in iron storage were demonstrable. The abnormal excretion of uroporphyrin and coproporphyrin were also brought under control. The success of treatment is attributed to the inhibitory effect of allopurinol on xanthine oxidase.

Adult↗

PubMed1995

Generation of free radicals by Cr(IV) from lipid hydroperoxides and its inhibition by chelators.

The generation of free radicals by Cr(IV) from lipid hydroperoxides was investigated by ESR spin trapping. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Reaction of Cr(VI) with ascorbate was used as a source of Cr(IV). Incubation of Cr(VI) with ascorbate generated Cr(IV) and Cr(V). Addition of cumene hydroperoxide generated DMPO/R adduct with an enhancement of Cr(V) signal. Addition of Mn(II), whose function is to remove Cr(IV), caused dose-dependent inhibition of DMPO/R formation. Similar results were obtained using t-butyl hydroperoxide. Metal ion chelators, deferoxamine, 1,10-phenanthroline and diethylenetriaminepentaacetic acid inhibited DMPO/R formation in the order of deferoxamine > 1,10-phenanthroline > diethylenetriaminepentaacetic acid. The results suggest the possible role of Cr(IV) and its mediated free radical generation from lipid hydroperoxides in the mechanism of Cr(VI) carcinogenesis.

Ascorbic Acid↗

PubMed1994

Acquisition of iron bound to low molecular weight chelates by human monocyte-derived macrophages.

The iron content of tissue macrophages increases under conditions of elevated extracellular iron. Studies of macrophage iron acquisition have generally focused on iron uptake from transferrin via receptor-mediated endocytosis. However, in vivo macrophages are also exposed to extracellular low m.w. iron chelates, particularly under conditions of iron overload. Therefore, we examined the mechanism of iron acquisition from low m.w. chelates by human monocyte-derived macrophages. Iron acquisition was influenced by the nature of the iron chelate: Fe-ascorbate > Fe-citrate > Fe-nitrilotriacetate (NTA) = Fe-ADP > Fe-glycyl-L-histidyl-L-lysine > Fe-diethylenetriamine pentaacetic acid >> Fe-EDTA = Fe-deferoxamine. With the exception of Fe-EDTA and Fe-deferoxamine, iron acquisition was greater than that with diferric transferrin. As assessed by using iron acquisition from NTA as a model, the process is temperature dependent, but pH independent (pH 5 to 8), and is influenced by the medium in which the cells are suspended. Acquisition is not affected by NaF, 2-deoxy-D-glucose, NaCN, or monocyte-derived macrophage exposure to trypsin, pronase, phenylarsine oxide, dihydrocytochalasin B, filipin, nystatin, or digitonin. The rate of iron acquisition from NTA is induced by iron pre-exposure as well as aluminum. In contrast, NTA chelates of other transition metals (Cd, Cu, Ga, Mn, and Zn) inhibited iron uptake by 20 to 80%. Unlike results obtained with Ga-NTA, Ga(NO3)3 increased iron uptake from NTA. Data obtained with neutrophils, and undifferentiated U937 and HL-60 cells were similar, which suggests that myeloid cells share this pathway for iron acquisition. Iron acquisition via this mechanism may allow macrophages and other leukocytes to clear local states of iron overload in vivo.

Adenosine Triphosphate↗

PubMedDate not supplied

Vanadium(IV) causes 2'-deoxyguanosine hydroxylation and deoxyribonucleic acid damage via free radical reactions.

Vanadium(IV) caused molecular oxygen dependent 2'-deoxyguanosine (dG) hydroxylation to form 8-hydroxyl-2'-deoxyguanosine (8-OHdG). During a 15-minute incubation of 1.0 mM dG and 1.0 mM VOSO4 (vanadium(IV)) in phosphate buffer solution (pH 7.4) at room temperature under ambient air, dG was converted to 8-OHdG with a yield of about 0.31 percent. Catalase and formate inhibited the 8-OHdG formation while superoxide dismutase enhanced it. Diethylenetriaminepentaacetic acid (DTPA) and deferoxamine blocked the 8-OHdG formation. Incubation of vanadium(IV) with dG in argon did not generate any significant amount of 8-OHdG, indicating the role of molecular oxygen in the mechanism of vanadium(IV)-induced dG hydroxylation. Vanadium(IV) also caused molecular oxygen dependent deoxyribonucleic acid (DNA) strand breaks in a pattern similar to that observed for dG hydroxylation. Reaction of vanadium(IV) with H2O2 generated OH radicals, which were inhibited by DTPA and deferoxamine. Incubation of vanadium(IV) with dG or with DNA in the presence of H2O2 resulted in an enhanced 8-OHdG formation and substantial DNA strand breaks. Reaction of vanadium(IV) with t-butyl hydroperoxide generated hydroperoxide-derived free radicals, which caused 8-OHdG formation from dG and DNA strand breaks.

Chelating Agents↗