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Results for “elevated iron concentrations”

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At least 19 recordsLinked to original sources

PubMed1997

Iron accumulation in lung allografts after transplantation.

Lung transplantation has become a therapeutic option for end-stage pulmonary diseases, but after transplantation, infections and obliterative bronchiolitis (OB) are major causes of long-term morbidity and mortality. OB is a fibroproliferative disease, of poorly understood etiology, characterized by an irreversible decline in allograft function. Because diseases with tissue iron overload are characterized by fibrosis and end-organ failure, we studied the iron concentrations in BAL fluid and lung tissue in 10 lung allograft patients. BAL fluid revealed significantly elevated iron concentrations in allograft patients compared with five normal volunteers (135+/-16.54 micromol/L vs 33.65+/-7.48 micromol/L, respectively). Prussian blue staining of biopsy specimens of lung allograft tissue revealed an accumulation of iron primarily in alveolar macrophages. Immunohistochemical stains for ferritin revealed accumulation of the protein in macrophages, interstitium, vascular walls, and bronchiolar epithelium. Iron studies of the blood (serum ferritin and iron concentrations) revealed no evidence for systemic iron overload. In conclusion, patients with pulmonary allografts appear to have elevated concentrations of iron in lung tissue. This iron overload may place the allografts at increased risk of metal-mediated injury and fibrosis.

Adult↗

PubMed1988

Elevated serum iron concentration in adolescent alcohol users.

Alcohol is a frequently abused drug among adolescents. In adults, alcohol alters iron metabolism, predisposing to excess hepatic iron storage and, possibly, liver damage. The purpose of this study was to determine whether alcohol is associated with an elevated serum iron concentration and transferrin saturation in adolescents, and to determine the contribution of oral contraceptive use to these abnormalities. Adolescents (591 male and 614 female) aged 16 to 19 years, who participated in the first National Health and Nutrition Examination Survey from 1971 to 1973, were grouped according to their reported frequency of alcohol intake. Drinking frequency was associated with serum iron concentrations in boys and girls, and with total iron-binding capacity, transferrin saturation, and hemoglobin concentration in boys. Alcohol use was associated with an elevated serum iron concentration only in oral contraceptive nonusers. Adolescents who use alcohol have an elevated serum iron concentration, and male alcohol users have an increased transferrin saturation as well. These abnormalities may be precursors of hepatic iron overload and chronic liver damage.

Adolescent↗

PubMed2001

Elevated iron status increases bacterial invasion and survival and alters cytokine/chemokine mRNA expression in Caco-2 human intestinal cells.

Iron status affects both microbial growth and immune function. Mammalian iron homeostasis is maintained primarily by regulating the absorption of the micronutrient in the proximal small intestine. The iron concentration of the enterocyte can fluctuate widely in response to both dietary and whole body iron status, as well as in response to infections. The possibility that an enterocyte with an elevated iron concentration is more susceptible to invasion by enteric pathogens is not known. Therefore, we examined the impact of enterocyte iron status on the invasion and survival of an enteric pathogen, as well as on the levels of several cytokine and chemokine mRNAs by the host cell. The enterocyte-like Caco-2 human intestinal cell line and Salmonella enteritidis served as the models to examine the effect of iron on the host-parasite interaction. Iron status of Caco-2 cells was altered by incubation in serum-free medium supplemented with varying levels of iron. Elevated iron status of Caco-2 cells increased the efficiency of the invasion and the number of bacteria surviving in the intracellular environment. Caco-2 cells constitutively expressed transforming growth factor-beta1, interleukin-8, monocyte chemotactic protein-1, tumor necrosis factor-alpha and interleukin-1beta, and infection with S. enteritidis increased the relative quantities of all cytokine/chemokine mRNAs except interleukin-1beta. Elevated iron status of Caco-2 cells decreased the levels of cytokine/chemokine mRNAs by 25-45% in uninfected cells. In contrast, bacterial infection was associated with a 21-95% increase in cytokine/chemokine mRNAs levels in Caco-2 cells with higher iron concentration compared with infected cells with lower iron concentration. These data support the hypothesis that elevated enterocyte iron status increases susceptibility to infection and exacerbates the mucosal inflammatory response initiated by microbial invasion by increasing cytokine/chemokine expression.

Analysis of Variance↗

PubMed2006

Tracer test with As(V) under variable redox conditions controlling arsenic transport in the presence of elevated ferrous iron concentrations.

To study transport and reactions of arsenic under field conditions, a small-scale tracer test was performed in an anoxic, iron-reducing zone of a sandy aquifer at the USGS research site on Cape Cod, Massachusetts, USA. For four weeks, a stream of groundwater with added As(V) (6.7 muM) and bromide (1.6 mM), was injected in order to observe the reduction of As(V) to As(III). Breakthrough of bromide (Br(-)), As(V), and As(III) as well as additional parameters characterizing the geochemical conditions was observed at various locations downstream of the injection well over a period of 104 days. After a short lag period, nitrate and dissolved oxygen from the injectate oxidized ferrous iron and As(V) became bound to the freshly formed hydrous iron oxides. Approximately one week after terminating the injection, anoxic conditions had been reestablished and increases in As(III) concentrations were observed within 1 m of the injection. During the observation period, As(III) and As(V) were transported to a distance of 4.5 m downgradient indicating significant retardation by sorption processes for both species. Sediment assays as well as elevated concentrations of hydrogen reflected the presence of As(V) reducing microorganisms. Thus, microbial As(V) reduction was thought to be one major process driving the release of As(III) during the tracer test in the Cape Cod aquifer.

Arsenic↗

PubMed2002

Hemochromatosis detection in a health screening program at an Alabama forest products mill.

We analyzed hemochromatosis detection in a 11.5-year multiphasic health screening program at a forest products mill. There were 2199 participants: 2032 Whites (1506 men, 526 women) and 167 African Americans (124 men, 43 women); 85.0% of employees were screened. Iron and transferrin saturation were measured in a serum biochemistry profile on specimens obtained after overnight fasting; ferritin was measured in participants with elevated iron concentrations or transferrin saturation > 48%. Participants with elevated ferritin levels underwent further evaluation. Eight White men were diagnosed to have hemochromatosis (frequency 0.0039 in Whites, 0.0053 in White men). The estimated cost per case detected was $8826. Family members of two participants with hemochromatosis were also diagnosed to have hemochromatosis or iron overload. We conclude that detecting hemochromatosis in a workplace multiphasic health screening program is efficacious and economical.

Adult↗

PubMed2005

Blood manganese concentration is elevated in iron deficiency anemia patients, whereas globus pallidus signal intensity is minimally affected.

OBJECTIVES: To determine whether blood manganese (Mn) concentration is elevated in patients with iron deficiency anemia (IDA), and whether this affects signal intensities in the globus pallidus. METHODS: Twenty-seven patients with IDA and 10 control subjects were tested for blood Mn, and brain magnetic resonance images (MRI) were also examined. Seventeen of the 27 patients were followed-up after iron therapy. RESULTS: IDA patients had a mean blood Mn concentration of 2.05 +/- 0.44 microg/dl, which was higher than controls. The mean pallidal index (PI) of anemic patients was not different from that of controls. There was a correlation between log blood Mn and PI (rho = 0.384, P = 0.048; n = 27) in IDA patients. None of the patients showed increased signals in the globus pallidus in T1-weighted MRI. Blood Mn levels decreased and hemoglobin levels increased after iron therapy (P < 0.05). CONCLUSION: Although blood Mn is elevated in IDA patients, there is no increase in globus pallidus MRI signal intensity. These findings stand in contrast to those of our other studies showing patients with chronic liver disease or occupational Mn exposure have elevated signal intensities remarkably.

Adult↗

PubMed1971

Iron requirements and aluminum sensitivity of an hydroxamic acid-requiring strain of Bacillus megaterium.

Bacillus megaterium strain ATCC 19213 secretes a ferric-chelating secondary hydroxamic acid, whereas a mutant (strain SK11) derived from it cannot produce a hydroxamate. Strain SK11 could be cultivated in a sucrose-mineral salts medium (treated with Chelex 100 to reduce trace metals) in the absence of added hydroxamate, if the inoculum was high. The lowest iron supplements necessary for maximal growth of both strains were equivalent (0.01 to 0.04 mug of iron per ml). Addition of either aluminum (0.5 mug/ml) or chromium (0.1 mug/ml) to the medium prevented full growth of strain SK11 at the minimal iron concentration, although elevated iron (1 mug/ml) reversed this inhibition. The iron-free secondary hydroxamate, Desferal, also abolished aluminum and chromium inhibition of strain SK11, producing maximal population densities at the low iron concentration. Growth of the hydroxamate-producing strain 19213 was not altered significantly by the aluminum or chromium levels which inhibited strain SK11. However, strain 19213 responded to these metals by increasing its secretion of a secondary hydroxamate. It was concluded that aluminum and chromium interfered with iron incorporation, either directly or by formation of nonutilizable aggregates with iron. The secondary hydroxamates may have overcome this interference by solubilization of iron for delivery to a single uptake process, or the ferric-hydroxamate chelate may enter the cell by an alternate route.

Aluminum↗

PubMed1991

Does iron affect osteoblast function? Studies in vitro and in patients with chronic liver disease.

In order to study the role of trace elements as potential osteoblastic toxins, we measured bone aluminum, copper, and iron in 106 ambulant patients with histologically proven liver disease. We used analytical and histochemical methods and we correlated our results with serum biochemistry, forearm and spinal bone density, and dynamic bone histomorphometry. Patients with chronic liver disease had higher iron-stained perimeters than control subjects (P less than 0.001). However, the mean iron-stained perimeter was no greater than 5% of the total mineralized bone perimeter and did not correlate significantly with either the osteoblast perimeters or bone formation rates. The mean concentration of bone iron were 2.5 times (P less than 0.01) greater in the patients than in the controls although 80% of the patients fell within the normal range. There was a weak negative correlation between bone iron and the osteoblast perimeters (R = 0.18, P = ns) and between bone iron and bone formation (R = -0.30, P less than 0.05). There were 57 patients (56% of the total) with diminished bone formation, but only 16 had elevated bone iron concentrations. In a regression analysis, age, hypogonadism, and serum albumin concentrations were the most important predictors of osteoblast perimeters and bone formation rates. In vitro experiments using rat osteoblast-like osteosarcoma cells showed that an iron concentration of 400 mumol/liter was required to diminish cellular proliferation and function. Iron concentrations are elevated in the bones of patients with chronic liver disease. However, there is at present insufficient evidence that this metal is responsible for the osteoblast dysfunction seen in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Elevated serum bleomycin-detectable iron concentrations in patients with sepsis syndrome.

OBJECTIVE: To determine serum bleomycin-detectable ¿free' iron in patients with septic shock and to relate these findings to both outcome and a marker of free radical damage. DESIGN: A prospective observational study. SETTING: A nine-bed intensive care unit in a university teaching hospital. PATIENTS: Sixteen consecutive patients with septic shock, defined as: (1) Clinical evidence of acute infection; (2) hypo- or hyperthermia ( < 35.6 degrees or > 38.3 degrees C); (3) tachypnoea ( > 20 breaths/min or ventilated); (4) tachycardia ( > 90 beats min); (5) shock (systolic pressure < 90mmHg) or on inotropes. Fourteen patients also had secondary organ dysfunction. MEASUREMENTS AND RESULTS: Bleomycin-detectable iron concentrations were elevated in all patients (37.2 +/- 11.0 mumols/l vs 5.1 +/- 3.3 mumols/l in healthy subjects, P < 0.0001), but there was no difference between patients who died and those who survived (39.2 +/- 9.3 and 36.2 +/- 12.3 mumols/l, respectively). Thiobarbituric acid reactive substances (an index of lipid peroxidation) were higher in those who died (3.33 +/- 2.29 mumols/l) than in the surviving patients (0.99 +/- 0.14 mumols/l, P < 0.01) or healthy subjects (0.92 +/- 0.39 mumols/l, P < 0.01). Free iron did not correlate with thiobarbituric acid-reactive substances. However, a significant correlation was found between lipid peroxidation and clinical severity (APACHE II) score (r = 0.54, P < 0.05). CONCLUSIONS: The present study provides evidence of lipid peroxidation in patients who die with septic shock. The data suggest that iron-catalysed hydroxyl radical generation does not form an important contribution to this lipid peroxidation in patients with sepsis.

APACHE↗

PubMed2006

[Molecular genetic diagnostics and screening of hereditary hemochromatosis].

BACKGROUND: Hereditary hemochromatosis is considered one of the most common hereditary diseases in population of Caucasian origin. In recent years, a candidate gene for HLA-linked hemochromatosis, HFE, has been cloned, and a single G-to-A mutation resulting in a cysteine-to-tyrosine substitution (C282Y) has been identified in up to 80% of study patients with type 1 hereditary hemochromatosis. The purpose of the paper was to confirm the importance of genetic testing for HFE mutations in making the diagnosis of hemochromatosis and find out a suitable diagnostic algorithm for the indication of this form of diagnostics in patients suspected of hereditary hemochromatosis. PATIENTS AND METHODS: The examination of C282Y mutation was conducted in 500 subjects. The most frequent indications for DNA analysis were hepatopathy of unknown ethiology, liver cirrhosis, diabetes mellitus, bronze skin pigmentation in connection with high serum iron concentration, elevated transferrin saturation and elevated serum ferritin levels. RESULTS: In our group of patients, 29 homozygotes and 75 heterozygotes for C282Y mutation were identified, 10 patients carried both C282Y and H63D mutations of HFE gene (compound heterozygotes), whereas in 386 subjects the mutation was not found. The genotype-phenotype correlation showed that 22 homozygotes had liver affection proved by imaging and/or histologic methods. Except the liver disorders, the most common symptoms of these patients were type 2 diabetes mellitus or glucose tolerance disorder (10 patients), arthritis or joint pain (9 patients) and cardiovascular disorders, such as cardiomyopathy (2 patients). Bronze skin pigmentation was present in 9 homozygotes. Transferin saturation values were significantly higher in homozygotes for C282Y mutation as compared to C282Y heterozygotes (p < 0.001), C282Y/H63D compound heterozygotes (p < 0.05) or wild type subjects (p < 0.001) respectively. Also serum ferritin levels were significantly higher in homozygotes for C282Y mutation as compared to C282Y heterozygotes (p < 0.001), C282Y/H63D compound heterozygotes (p < 0.001) and wild type subjects (p < 0.001) respectively. CONCLUSIONS: Our observations confirm that DNA analysis significantly contributes to differential diagnostics of this severe, but in early recognition curable disease. Early detection and phlebotomy treatment prior to the onset of cirrhosis can reduce morbidity and normalize life expectancy. It is readily identified through biochemical testing for iron overload using serum transferrin saturation and genetic testing for C282Y homozygosity. DNA analysis is recommended in patients whose transferrin saturation is 45% or more on a repeated test. General population screening has been waived in preference to targeting high-risk groups such as first-degree relatives of affected individuals and those with secondary iron overload, especially patients with chronic liver disorders and chronic anemia. This screening strategy is likely to continue until uncertainties regarding the natural history of the disease, age-related penetrance, and management of asymptomatic individuals are clarified.

Adolescent↗

PubMed1994

Complex I, iron, and ferritin in Parkinson's disease substantia nigra.

Elevated iron levels, enhanced oxidative damage, and complex I deficiency have been identified in the substantia nigra of Parkinson's disease patients. To understand the interrelationship of these abnormalities, we analyzed iron levels, ferritin levels, and complex I activity in the substantia nigra of patients with Parkinson's disease. Total iron levels were increased significantly, ferritin levels were unchanged, and complex I activities were decreased significantly in the substantia nigra samples. The failure of ferritin levels to increase with elevated iron concentrations suggests that the amount of reactive iron may increase in the substantia nigra of Parkinson's disease patients. There was no correlation between the iron levels and complex I activity or the iron-ferritin ratio and complex I activity in the substantia nigra samples.

Aged↗

PubMed1984

Thermostable erythrocyte rosette-forming lymphocytes in hereditary hemochromatosis. I. Identification in peripheral blood.

Although the immunoregulatory role of iron has been demonstrated in vitro, evidence for a similar role in vivo is controversial. We have, therefore, studied certain functional and structural properties of lymphocytes in hereditary (idiopathic) hemochromatosis (HH), a disease characterized by iron overload. T- and B-lymphocyte percentages in peripheral blood, serum immunoglobulin levels, and proliferative responses of peripheral blood mononuclear cells (PBM) to lectins were comparable with those of controls. Furthermore, HH serum with elevated iron concentrations did not significantly alter proliferative responses of normal lymphocytes to mitogens. In contrast to those normal findings was the identification of a subset of T lymphocytes in HH that formed rosettes with sheep red blood cells (SRC) at 37 degrees C in abnormally high numbers. Those lymphocytes that formed thermostable erythrocyte rosettes (TE-R) were not immature thymocytes, activated T lymphocytes, or an artifact of passive attachment of anti-SRC antibodies to the HH lymphocyte surface. Their presence did not correlate with a concentration of iron in the serum, the length of treatment, or the presence of the HLA antigen, A3. We conclude that the cellular expression of HH may be detected not as an immunological abnormality, but rather as an abnormality in receptor expression.

Antibodies, Monoclonal↗

PubMed2005

Iron salts perturb biofilm formation and disrupt existing biofilms of Pseudomonas aeruginosa.

Bacterial biofilms are thought to aid in the survivability of a variety of intractable infections in humans. Specifically, biofilm production in Pseudomonas aeruginosa has been shown to play a significant role in chronic infection of cystic fibrosis (CF) patients. Unfortunately, no clinically effective inhibitors of biofilm formation are available. A rapid screen of 4509 compounds for nonantibiotic biofilm inhibitors in Pseudomonas aeruginosa PA14 was executed in 384-well plates. Among those compounds, ferric ammonium citrate inhibited biofilm formation in a dose-dependent manner; other iron salts functioned similarly. In addition to biofilm inhibition in static culture, pregrown biofilms could be disrupted and cleared by switching to iron-rich media in flow-chamber experiments. Furthermore, P. aeruginosa strains taken from the sputum of 20 CF patients showed a similar response to elevated iron levels. Previous expression-profiling analyses demonstrated that high levels of iron repress the expression of genes whose products are essential for scavenging iron and that expression of these genes is critical for virulence. Our results, combined with existing transcriptional-profiling data, now indicate that elevated iron concentrations repress the expression of certain genes essential for biofilm production in P. aeruginosa.

Biofilms↗

PubMed2003

The Schizosaccharomyces pombe corepressor Tup11 interacts with the iron-responsive transcription factor Fep1.

The Schizosaccharomyces pombe fep1(+) gene encodes a GATA transcription factor that represses the expression of iron transport genes in response to elevated iron concentrations. This transcriptional response is altered only in strains harboring a combined deletion of both tup11(+) and tup12(+) genes. This suggests that Tup11 is capable of negatively regulating iron transport gene expression in the absence of Tup12 and vice versa. The tup11(+)- and tup12(+)-encoded proteins resemble the Saccharomyces cerevisiae Tup1 corepressor. Using yeast two-hybrid analysis we show that Tup11 and Fep1 physically interact with each other. The C-terminal region from amino acids 242 to 564 of Fep1 is required for interaction with Tup11. Within this region, a minimal domain encompassing amino acids 405-541 was sufficient for Tup11-Fep1 association. Deletion mapping analysis revealed that the WD40-repeat sequence motifs of Tup11 are necessary for its interaction with Fep1. Analysis of Tup11 mutants with single amino acid substitutions in the WD40 repeats suggested that the Fep1 transcription factor interacts with a putative flat upper surface on the predicted beta-propeller structure of this motif. Further analysis by in vivo coimmunoprecipitation showed that Tup11 and Fep1 are physically associated. In vitro pull-down experiments further verified a direct interaction between the Fep1 C terminus and the Tup11 C-terminal WD40 repeat domain. Taken together, these results describe the first example of a physical interaction between a corepressor and an iron-sensing factor controlling the expression of iron uptake genes.

Base Sequence↗

PubMed1982

Mechanical properties of the copper-deficient rat heart.

Copper deficiency is known to induce cardiac hypertrophy, cardiac morphologic lesions and altered electrocardiograms. These findings suggest that copper deficiency may also influence the mechanical properties of the myocardium. In the present study, weanling albino rats were fed a copper-deficient (-Cu) diet and compared to rats fed the same diet but with copper supplementation in the drinking water (+Cu). Rats were studied during a 1-week period following 4.5-5.5 weeks of treatment. When compared to +Cu rats, the -Cu rats exhibited characteristic signs of copper deficiency, such as reduced body weight, hypoceruloplasminemia, depressed hematocrit, low copper and elevated iron concentration in the liver. The -Cu rats also exhibited cardiac hypertrophy and both a dilution and depletion of left ventricular norepinephrine. Hearts were perfused and paced at both 27 degrees and 37 degrees. When compared to hearts from +Cu rats, the -Cu hearts: 1) had lower spontaneous heart rates, 2) had decreased coronary resistance, 3) gained significant weight during perfusion, 4) consumed more oxygen per unit pressure developed, and 5) developed less systolic pressure with a reduced rate of pressure development. However, the time to peak pressure development, one-halt relaxation time, and refractory period were not affected. The altered characteristics of the copper-deficient myocardium may be due to changes in the elastic properties of the muscle, aberrant energy metabolism or norepinephrine depletion.

Animals↗

PubMed1991

Intranigral iron injection induces behavioral and biochemical "parkinsonism" in rats.

Elevated iron concentrations in the substantia nigra (SN) pars compacta have been implicated in the development of idiopathic Parkinson's disease. Because, as a transitional metal, iron promotes free radical formation, the role of iron in the degeneration of the nigrostriatal dopamine neurons in Parkinson's disease has received much attention. This study further investigates the cytotoxic effects of iron in the SN. Various concentrations of FeCl3 (1, 5, and 50 micrograms of Fe3+ in 5 microliters) were unilaterally injected into the SN of adult rats. The two lower doses of iron had no effect on striatal dopamine levels or on the behavioral responses of the rats. However, injection of 50 micrograms of Fe3+ resulted in a substantial selective decrease of striatal dopamine (95%), 3,4-dihydroxyphenylacetic acid (82%), and homovanillic acid (45%), without any change in norepinephrine concentration. Dopamine-related behavioral responses, such as spontaneous movements in a novel space and rearing, were significantly impaired, whereas amphetamine administration induced ipsilateral rotation in the iron-treated rats. The present study indicates that the nigrostriatal dopamine neurons are susceptible to the presence of ionic iron and thus supports the assumption that iron initiates dopaminergic neurodegeneration in Parkinson's disease.

Animals↗

PubMed2001

PerR controls oxidative stress resistance and iron storage proteins and is required for virulence in Staphylococcus aureus.

The Staphylococcus aureus genome encodes three ferric uptake regulator (Fur) homologues: Fur, PerR, and Zur. To determine the exact role of PerR, we inactivated the gene by allelic replacement using a kanamycin cassette, creating strain MJH001 (perR). PerR was found to control transcription of the genes encoding the oxidative stress resistance proteins catalase (KatA), alkyl hydroperoxide reductase (AhpCF), bacterioferritin comigratory protein (Bcp), and thioredoxin reductase (TrxB). Furthermore, PerR regulates transcription of the genes encoding the iron storage proteins ferritin (Ftn) and the ferritin-like Dps homologue, MrgA. Transcription of perR was autoregulated, and PerR repressed transcription of the iron homeostasis regulator Fur, which is a positive regulator of catalase expression. PerR functions as a manganese-dependent, transcriptional repressor of the identified regulon. Elevated iron concentrations produced induction of the PerR regulon. PerR may act as a peroxide sensor, since addition of external hydrogen peroxide to 8325-4 (wild type) resulted in increased transcription of most of the PerR regulon, except for fur and perR itself. The PerR-regulated katA gene encodes the sole catalase of S. aureus, which is an important starvation survival determinant but is surprisingly not required for pathogenicity in a murine skin abscess model of infection. In contrast, PerR is not necessary for starvation survival but is required for full virulence (P < 0.005) in this model of infection. PerR of S. aureus may act as a redox sentinel protein during infection, analogous to the in vitro activities of OxyR and PerR of Escherichia coli and Bacillus subtilis, respectively. However, it differs in its response to the metal balance within the cell and has the added capability of regulating iron uptake and storage.

Amino Acid Sequence↗

PubMed1973

Hydroxamate recognition during iron transport from hydroxamate-ion chelates.

Kinetics of radioactive iron transport from three structurally different secondary hydroxamate-iron chelates (schizokinen-iron, produced by Bacillus megaterium ATCC 19213; Desferal-iron, produced by an actinomycete; and aerobactin-iron, produced by Aerobacter aerogenes 62-1) revealed that B. megaterium SK11 (a mutant which cannot synthesize schizokinen) has a specific transport system for utilization of ferric hydroxamates with a recognition capacity based on the chemical structure of the hydroxamate. Both Desferal and schizokinen enhanced iron uptake in this organism; however, Desferal-iron delivered only one-sixth the level of iron incorporated from the schizokinen-iron chelate. Desferal-iron did not generate the rapid rates of iron transport noted with schizokinen-iron at elevated iron concentrations. Assays containing large excesses of either iron-free Desferal or iron-free schizokinen suggested that the iron-free hydroxamate may compete with the ferric hydroxamate for acceptance by the transport system although the system has greater affinity for the iron chelate. Aerobactin-iron did not stimulate iron uptake in B. megaterium SK11 and aerobactin inhibited growth of this organism, indicating that B. megaterium SK11 cannot efficiently process the aerobactin-iron chelate.

Bacillus megaterium↗