Bibliografías temáticas / Iron Metabolism

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Literatura académica sobre el tema "Iron Metabolism"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 7 de julio de 2024

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Artículos de revistas sobre el tema "Iron Metabolism"

1

Conway, Deirdre y Mark A. Henderson. "Iron metabolism". Anaesthesia & Intensive Care Medicine 23, n.º 2 (febrero de 2022): 123–25. http://dx.doi.org/10.1016/j.mpaic.2021.10.021.

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COUGHLAN, MICHAEL P. "Iron Metabolism". Biochemical Society Transactions 13, n.º 4 (1 de agosto de 1985): 803. http://dx.doi.org/10.1042/bst0130803.

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Aisen, Philip, Marianne Wessling-Resnick y Elizabeth A. Leibold. "Iron metabolism". Current Opinion in Chemical Biology 3, n.º 2 (abril de 1999): 200–206. http://dx.doi.org/10.1016/s1367-5931(99)80033-7.

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Conway, Deirdre y Mark A. Henderson. "Iron metabolism". Anaesthesia & Intensive Care Medicine 20, n.º 3 (marzo de 2019): 175–77. http://dx.doi.org/10.1016/j.mpaic.2019.01.003.

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Badwing, TP. "Iron Metabolism". Biochemical Education 13, n.º 3 (julio de 1985): 150. http://dx.doi.org/10.1016/0307-4412(85)90229-8.

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Ponka, Prem. "Cellular iron metabolism". Kidney International 55 (marzo de 1999): S2—S11. http://dx.doi.org/10.1046/j.1523-1755.1999.055suppl.69002.x.

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Anderson, Gregory J. y David M. Frazer. "Hepatic Iron Metabolism". Seminars in Liver Disease 25, n.º 04 (2005): 420–32. http://dx.doi.org/10.1055/s-2005-923314.

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Rouault, Tracey A. y Sharon Cooperman. "Brain Iron Metabolism". Seminars in Pediatric Neurology 13, n.º 3 (septiembre de 2006): 142–48. http://dx.doi.org/10.1016/j.spen.2006.08.002.

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Valerio, Luis G. "Mammalian Iron Metabolism". Toxicology Mechanisms and Methods 17, n.º 9 (enero de 2007): 497–517. http://dx.doi.org/10.1080/15376510701556690.

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Kohgo, Yutaka. "2. Iron Metabolism and Iron Overload." Nihon Naika Gakkai Zasshi 100, n.º 9 (2011): 2412–24. http://dx.doi.org/10.2169/naika.100.2412.

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Tesis sobre el tema "Iron Metabolism"

1

SAITO, HIROSHI. "METABOLISM OF IRON STORES". Nagoya University School of Medicine, 2014. http://hdl.handle.net/2237/20543.

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Alvarez-Hernandez, J. "Iron metabolism in macrophages". Thesis, University of Glasgow, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375442.

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Xue, Yue 1978. "Iron metabolism in mammalian cells". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79216.

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Iron, known for its versatility, is an essential element in the metabolism of mammalian cells. One of the most common iron disorders is autosomal recessive disease---hereditary hemochromatosis, which leads to the iron overload in population of northern European descent. During years of my graduate research, I focused on the study of Hemochromatosis gene Hfe and a point mutation C282Y that leads to more than 80% of all hemochromatosis cases.
Iron Regulatory Proteins (IRPs), which serve as main posttranscriptional regulators of cellular iron homeostasis, are the other interest of research. Iron regulatory proteins reversibly interact with iron regulatory elements (IREs) within ferritin and transferrin receptor (TfR) mRNAs. The binding ability of IRPs is under tight control so that they respond to the changes in the intracellular iron requirements in a coordinate manner by differentially regulating ferritin mRNA translational efficiency and TfR mRNA stability. Besides intracellular iron levels, some other stimuli, such as oxidative stress, are capable of regulating this RNA-protein interactions.
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Whitnall, Megan. "Iron metabolism, chelation and disease". Thesis, The University of Sydney, 2011. https://hdl.handle.net/2123/28914.

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Organisms depend on iron to survive. This fact is underscored by the critical requirement for iron during DNA synthesis and as a cofactor in proteins involved in respiration and oxygen transport. However, when present in excess of cellular requirements, iron can be toxic, due to its ability to generate reactive oxygen species and induce oxidative stress. The physiological significance of iron renders it a target for the development of iron chelators as therapeutic agents and highlights the potential problems that can occur when iron regulatory pathways are disturbed in disease. The rapid rate of neoplastic cell replication and the involvement of iron in cell cycle progression and DNA synthesis, highlight the potential for using iron chelators for cancer treatment. Chapter 3 of this thesis demonstrates the broad-spectrum in vitro and in vivo anti-tumour activity of the novel iron chelator, di-2-pyridylketone-4,4,-dimethyl-3-thiosemicarbazone (Dp44mT) (Whitnall et.al., Proc Natl Acad Sci USA 2006; 103:14901-6). In vitro results illustrate the potency of Dp44mT over the clinically used chemotherapeutic agent, doxorubicin, and the ability of Dp44mT to overcome multi­drug resistance. The unique ability of Dp44mT to up-regulate the tumour growth and metastasis suppressor, Ndrgl in in vivo experiments, may account for this ligands selective anti-tumour activity (Whitnall et al., 2006). Collectively, these studies demonstrate that iron chelators such as Dp44mT, may be valuable anti-cancer compounds, particularly considering the emergence of multi-drug resistance in tumours. There is no effective treatment for the cardiomyopathy of the most common autosomal recessive ataxia, Friedreich 's ataxia (FA). The identification of potentially toxic mitochondrial iron deposits in FA suggests iron plays a role in its pathogenesis and merits the use of iron chelation therapy for the treatment of FA. Studies in Chapters 4 and 5 used the muscle creatine kinase (MCK) frataxin mutant mouse model that reproduces the classical traits associated with cardiomyopathy in FA, to study the molecular alterations which underlie the pathogenesis of this disease and assess the use of iron chelation therapy (Whitnall et.al., Proc Natl Acad Sci USA 2008; 105:9757-62). Studies specifically in Chapter 4 show that the increased mitochondrial iron in the myocardium of mutants was due to marked transferrin-iron uptake, which was the result of enhanced transferrin receptor 1 (TfRl) expression. 1n contrast to the mitochondrion, cytosolic ferritin expression and the proportion of cytosolic iron were decreased in mutant mice, indicating the cytosol was iron deficient. These studies demonstrate that loss of frataxin alters cardiac iron metabolism due to pronounced changes in iron trafficking away from the cytosol to the mitochondrion. Further work in Chapter 4 showed that the mitochondrial-permeable ligand, pyridoxal isonicotinoyl hydrazone, in combination with the hydrophilic chelator, desferrioxamine, prevented cardiac iron loading and limited cardiac hypertrophy in mutants, but did not lead to overt cardiac iron depletion or toxicity (Whitnall et al., 2008). However, iron chelation did not prevent decreased succinate dehydrogenase expression in the mutants nor loss of cardiac function, indicating that frataxin function must also be replaced in addition to removing the excess mitochondrial iron. In summary, for the first time, studies in this thesis demonstrate that frataxin deficiency markedly alters cellular iron trafficking and that iron chelation limits myocardial hypertrophy in the MCK mutant model of FA. To address the cytosolic iron deficiency in the cardiomyocytes of mutant mice, in Chapter 5, mice were fed a high iron diet aimed at reconstituting the iron deprived cytosolic compartment. From these studies, a significant decrease in cardiac hypertrophy was observed in high iron diet fed mice. Interestingly, while wild-type (WT) mice responded to the high iron diet by decreasing cardiac TfRl expression, no such compensation was observed in high-compared to normal-iron iron diet fed mutants. Similarly, activity of iron regulatory protein 2 (i.e., IRP2 RNA-binding activity) was not decreased in high iron diet fed mutants. These findings demonstrate the mutant heart does not respond to increased iron levels as does the WT animal. An intriguing and important outcome of dietary iron loading investigations, was the marked increase in iron concentration observed in the liver, spleen and kidney of mutant mice that were fed a normal iron diet. The MCK mutant mouse experiences deletion of frataxin in the heart only, and hence, the increase in iron levels observed in frataxin ­intact tissues such as the liver, indicated that the heart is able to influence systemic iron metabolism. Supporting this, changes were observed in iron-metabolism proteins such as hemojuvelin and TfRl not only in the heart, but in the liver. Collectively, these results indicate that frataxin knockout in the heart and the alterations in iron metabolism which lead to cytosolic iron deficiency in the heart, activate a systemic signalling mechanism, most likely to communicate its need for iron within the cytosolic compartment. In the final section of Chapter 5, transmission electron microscopy and magnetic susceptibility measurements were used to assess the molecular composition of accumulated iron in the MCK mutants. These studies showed that the iron accumulating in the mutant heart is not present within ferritin, but in well crystallised anti­ferromagnetic mineral aggregates. In conclusion, the investigations described within this thesis demonstrate the potential for iron chelators to be used for the treatment of cancer and FA. Moreover, they also begin to elucidate the marked alterations in the pathways of iron metabolism that occur on both a cellular and systemic level in FA. ln terms of contributing to our understanding of basic physiological iron homeostasis, they also identify that cardiac iron status is able to markedly influence systemic iron metabolism.
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Ekins, Andrew John. "Iron acquisition by Histophilus ovis". Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38481.

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Five strains (9L, 642A, 714, 5688T and 3384Y) of Histophilus ovis were investigated with respect to iron acquisition. All strains used ovine, bovine and goat, but not porcine or human, transferrins (Tfs) as iron sources for growth. In solid phase binding assays, total membranes from only two (9L and 642A) of the five strains, grown under iron-restricted conditions, were able to bind Tfs (ovine, bovine and goat, but not porcine or human). However, when the organisms were grown under iron-restricted conditions in the presence of bovine Tf, total membranes from all strains exhibited Tf binding (as above); competition experiments demonstrated that all three Tfs (ovine, bovine and goat) were bound by the same receptor(s). An affinity isolation procedure allowed the isolation of two putative Tf-binding polypeptides (78 and 66 kDa) from total membranes of strains 9L and 642A grown under iron-restricted conditions, and from membranes of all strains if the growth medium also contained Tf. A gene encoding a Pasteurella multocida TbpA homologue was shown to be present in each of two representative strains (9L and 3384Y); these genes were sequenced and determined to be the structural genes encoding the 78-kDa Tf-binding polypeptides. The identification of a fur homologue and a Fur box within the promoter region of tbpA in both strains indicated that Fur (and iron) is responsible for the iron-repressible nature of Tf-binding activity. Although tbpA transcripts were detected by reverse transcription (RT)-PCR with RNA isolated from strains 9L and 3384Y grown under iron-restricted conditions, with strain 3384Y, and depending on the primer pair, tbpA transcripts were detected by RT-PCR predominantly when the RNA was isolated from cells grown under conditions of iron-restriction in the presence of Tf. The presence of an additional G in the tbpA gene of strain 3384Y grown under iron-replete conditions, compared to organisms grown under iron-restricted conditions plus bovine Tf, is
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Sritharan, Manjula. "Studies in iron metabolism of mycobacteria". Thesis, University of Hull, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278446.

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Lopes, Tiago Jose da Silva. "Systems biology analysis of iron metabolism". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16417.

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Jede Zelle des Säugetierorganismus benötigt Eisen als Spurenelement für zahlreiche oxidativ-reduktive Elektronentransfer-Reaktionen und für Transport und Speicherung von Sauerstoff. Der Organismus unterhält daher ein komplexes Regulationsnetzwerk für die Aufnahme, Verteilung und Ausscheidung von Eisen. Die intrazelluläre Regulation in den verschiedenen Zelltypen des Körpers ist mit einer globalen hormonellen Signalstruktur verzahnt. Sowohl Eisenmangel wie Eisenüberschuss sind häufige und ernste menschliche Krankheitsbilder. Sie betreffen jede Zelle, aber auch den Organismus als Ganzes. In dieser Dissertation wird ein mathematisches Modell des Eisenstoffwechsels der erwachsenen Maus vorgestellt. In ihm wird die Flussbilanz des Eisens in den wichtigsten Zelltypen in Form von transmembranalen und intrazellulären kinetischen Gleichungen dargestellt, und es werden diese Zellmodelle mit dem zentralen Eisenaustausch-Kompartiment (Blutplasma) des Körpers integriert. Der Eisenstatus wird charakterisiert als Gehalt an labil gebundenen Eisen und an ferritin-gebundenen Eisen für jede Zelle. Der Stoffwechsel wird als Netzwerk von Flussdynamik formuliert. Der experimentelle Input in dieses Modells stammt von verschiedenen Quellen. Radioaktive Tracerdaten, gemessen am intakten Tier (Mausstamm C57BL6 – das am intensivsten studierte Tiermodell) unter varrierten physiologischen Bedingungen lieferten den experimentellen Hintergrund, von dem aus Clearance-Parameter durch numerisches Fitting ermittelt wurden. Es wird gezeigt, dass das Modell mit entsprechend adaptierten Parametersätzen die wichtigsten metabolischen und regulatorischen Ereignisse in Übereinstimmung mit den Messungen darstellen kann. In Zukunft soll die quantitative Übereinstimmung mit Daten aus weiteren genetischen Rekonstruktionen (globale und zell-spezifische knock-outs und konstitutive Expression relevanter Gene des Modellorganismus Maus) hergestellt werden.
Every cell of the mammalian organism needs iron as trace element in numerous oxido-reductive processes as well as for transport and storage of oxygen. The mammalian organism maintains therefore a complex regulatory network of iron uptake, excretion and intra-body distribution. Here a mathematical model of iron metabolism of the adult mouse is presented. It formulates the iron flux balance of the most important cell types of the organism in the form of transmembraneous and intracellular kinetic equations and integrates these cell models with the central exchange compartment (blood plasma) of the body. The iron status is represented as content of labile iron and of ferritin-bound iron in every cell type, and the metabolism is formulated as a network of flux dynamics. The experimental input into the model stems from different sources. Radioactive tracer data measured in the intact animal (mouse strain C57BL6 - the most intensively studied animal model) under various physiological conditions provided the experimental background from which clearance parameters could be obtained by numerical parameter fitting. Future research should render more precise the quantitative representation of genetic reconstructions (global and cell-type-addressed knock-out and constitutive expression of relevant genes of the model mouse strain).
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Bahrami, Fariborz. "Iron acquisition in Actinobacillus suis". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85880.

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Seven strains of Actinobacillus suis (ATCC 15557, B49, C84, H89-1173, H91-0380, SO4 and VSB 3714) were investigated with respect to iron acquisition from animal transferrins (Tfs) and haemoglobins (Hbs). Growth assays with porcine, bovine and human Tfs and Hbs revealed that all seven strains could use porcine (but not human or bovine) Tf and all three Hbs as iron sources. In solid phase binding assays, membranes derived from all strains exhibited strong binding of porcine Tf and each of the Hbs. Competition binding assays indicated that all three Hbs were bound by the same receptor(s). Affinity procedures allowed the isolation and identification of iron repressible Tf-binding (~100 kDa and ~63 kDa) and Hb-binding (~105 kDa) polypeptides from all strains. Nucleotide sequence analyses revealed that A. suis strains SO4 and C84 possess genes that encode homologues of the Actinobacillus pleuropneumoniae Tf-binding proteins, TbpA and TbpB, and Hb-binding protein, HgbA. In both strains, tbpB was located immediately upstream of tbpA and was shown to be preceded by tonB, exbB and exbD homologues; hgbA was shown to be preceded by a hugZ homologue. Putative promoter and Fur box sequences were located upstream of tonB and hugZ and RT-PCR revealed that the genes in each of these clusters (tonB-exbB-exbD-tbpB-tbpA; hugZ-hgbA) are co-transcribed and iron-repressible. The molecular masses of the predicted mature TbpA, TbpB and HgbA proteins were calculated to be 104.3, 63.4 and 105.0 kDa, respectively, suggesting that the affinity-isolated, ~100 kDa and ~63 kDa Tf-binding polypeptides represent TbpA and TbpB, respectively, and that the ~105 kDa Hb-binding polypeptide represents HgbA. TbpB of A. suis was expressed in Escherichia coli and the recombinant TbpB (rTbpB) was identified by immunoblotting using swine sera raised against recombinant TbpB (A. pleuropneumoniae). It is envisaged that the acquisition of Tf- and Hb-bound iron by A. suis involves mechan
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Bae, Dong-Hun. "The Effects of Iron Levels on the Interaction between Polyamine Metabolism and Iron Metabolism in Neoplastic Cells". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/18081.

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Iron is a crucial element that is associated with many metabolic pathways important for life sustaining processes. Polyamines are small positively charged polycations involved in various physiological functions. Both iron and polyamines levels are known to be high in cancer cells which suggests a possible unexplored link between the two metabolic pathways. For the first time, we demonstrate that iron-depletion robustly regulates the expression of 13 polyamine pathway proteins. Iron-depletion also decreased polyamine and S-adenosylmethionine levels (required for spermidine/spermine biosynthesis) and decreased 3H-spermidine uptake in accordance with expression of the polyamine importer, SLC22A16. The “reprogramming” of polyamine metabolism by iron-depletion showed dependence on the proto-oncogene, c-Myc, and tumour suppressor, p53 expression. Furthermore, the ability of iron chelators to inhibit proliferation can be rescued by polyamine supplementation. Collectively, these data demonstrate that iron and polyamine metabolism are closely linked at multiple levels. Moreover, we have identified that the mRNA and protein expression of the iron-containing enzyme, aci-reductone dioxygenase 1 (ADI1), was regulated by iron levels. Cellular iron depletion or deficient ADI1 metalation by the iron chaperone, PCBP1, promotes the proteasomal degradation of ADI1. Collectively, this demonstrates that cellular iron regulates ADI1 stability, a key enzyme involved in methionine salvage, polyamine biosynthesis and proliferation. In addition to regulating ADI1, poly(rC)-binding proteins (PCBPs) have been reported to function as iron-binding chaperones that deliver iron to ferritin. We observed that PCBP2 enhances, while PCBP1 inhibits ferritin 59Fe-loading and ferritin protein expression. Our results suggest that the regulation of ferritin iron-loading by PCBPs may involve a combination of translational regulation and/or iron chaperone activity. Overall this study has demonstrated for the first time the direct interaction between iron metabolism and polyamine metabolism, which is important in understanding how cancer cells can survive adverse environments.
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Tremblay, Yannick. "Acquisition of haemoglobin-bound iron by Histophilus somni". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82441.

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Ovine (strains 9L and 3384Y) and bovine (strains 649, 2336 and 8025) isolates of Histophilus somni were investigated for their ability to acquire iron from haemoglobin (Hb). Bovine isolates were capable of utilizing bovine, but not ovine, porcine or human Hb as a source of iron. Ovine isolates could not obtain iron from Hb. Bovine isolates bound bovine, ovine, and human Hbs by means of the same iron-repressible receptor(s) and produced a ~120-kDa iron-repressible, outer membrane protein. Using PCR approaches, an iron-regulated operon containing hugX and hugZ homologues and a gene (hgbA) that encodes a TonB-dependent, Hb-binding proteins were identified in strains 649, 9L and 3384Y. In strains 9L and 3384Y, HgbA is truncated offering a possible explanation for their lack of utilization of Hb as an iron source. In strains 2336 and 8025, expression of HgbA was also subject to a form of phase variation.
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Libros sobre el tema "Iron Metabolism"

1

Crichton, Robert. Iron Metabolism. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118925645.

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Mark, Worwood, ed. Iron metabolism. London: Baillière Tindall, 2002.

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Wick, Manfred, Wulf Pinggera y Paul Lehmann. Ferritin in Iron Metabolism. Vienna: Springer Vienna, 1995. http://dx.doi.org/10.1007/978-3-7091-4421-3.

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Wick, Manfred, Wulf Pinggera y Paul Lehmann. Ferritin in Iron Metabolism. Vienna: Springer Vienna, 1991. http://dx.doi.org/10.1007/978-3-7091-4435-0.

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Proteins of iron metabolism. Boca Raton, Fla: CRC Press, 2002.

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1938-, Lönnerdal Bo, ed. Iron metabolism in infants. Boca Raton, Fla: CRC Press, 1990.

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Crichton, Robert R. Inorganic biochemistry of iron metabolism. New York: E. Horwood, 1991.

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C, Hershko, ed. Clinical disorders of iron metabolism. London: Baillière Tindall, 1994.

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C, Ferreira Glória, Moura José J. G y Franco Ricardo, eds. Iron metabolism: Inorganic biochemistry and regulatory mechanisms. Weinheim: Wiley-VCH, 1999.

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Chang, Yan-Zhong, ed. Brain Iron Metabolism and CNS Diseases. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9589-5.

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Capítulos de libros sobre el tema "Iron Metabolism"

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Koscielny, J. y H. Kiesewetter. "Iron Metabolism". En Hemodilution, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-662-07748-1_1.

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Wick, Manfred, Wulf Pinggera y Paul Lehmann. "Iron Metabolism". En Clinical Aspects and Laboratory — Iron Metabolism, Anemias, 3–16. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0087-5_2.

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Wick, Manfred, Paul Lehmann y Wulf Pinggera. "Iron Metabolism". En Clinical Aspects and Laboratory Iron Metabolism, Anemias, 2–16. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-3719-2_2.

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Fellman, Vineta. "Iron Metabolism Disorders". En Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 633–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40337-8_40.

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Ponka, Prem y Alex D. Sheftel. "Erythroid Iron Metabolism". En Iron Physiology and Pathophysiology in Humans, 191–209. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-485-2_10.

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Philpott, Caroline C. "Yeast Iron Metabolism". En Iron Physiology and Pathophysiology in Humans, 653–67. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-485-2_30.

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Youdim, M. B. H. "Brain Iron Metabolism". En Pathological Neurochemistry, 731–55. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-0797-7_27.

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Bradeen, Heather, Samir Shehab y Michael Recht. "Iron Metabolism and Iron Deficiency Anemia". En Textbook of Clinical Pediatrics, 2963–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_318.

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Sikka, Meera y Harresh B. Kumar. "Iron Metabolism and Iron Deficiency Anemia". En Hematopathology, 27–47. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7713-6_2.

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Wick, Manfred, Wulf Pinggera y Paul Lehmann. "Disturbances of Iron Metabolism". En Ferritin in Iron Metabolism, 14–17. Vienna: Springer Vienna, 1991. http://dx.doi.org/10.1007/978-3-7091-4435-0_3.

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Actas de conferencias sobre el tema "Iron Metabolism"

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Hassenkam, Tue, Ester Tsai, Henning Osholm, Kim Dalby, David Mackenzie, Mirko Holler, Dario Ferreira, Daniel Grolimund, Stephan Bruns y Minik T. Rosing. "Eoarchean Iron Metabolism?" En Goldschmidt2020. Geochemical Society, 2020. http://dx.doi.org/10.46427/gold2020.973.

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Schonberg, David L. y Jeremy N. Rich. "Abstract 5205: Iron metabolism informs glioblastoma stem cell maintenance". En Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5205.

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Mayall, J., A. Pillar, K. Daly, A. Brown, A. Essilfie, H. Gomez, R. Kim et al. "Iron metabolism determines the outcome of influenza A virus infection". En ERS Lung Science Conference 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.lsc-2023.71.

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Theobald, Vivienne, Ekkehard Grünig, Nicola Benjamin, Benjamin Egenlauf, Henning Gall, Ardeschir Ghofrani, Michael Halank et al. "BMPR2 mutations and iron metabolism in pulmonary arterial hypertension patients". En ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa587.

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Pencheva Genova, Ventsislava, Victor Manolov, Ognian Gerogiev, Vasil Vasilev, Savina Hadjidekova, Latchezar Traykov y Kamen Tzatchev. "Disregulation of iron metabolism and atherosclerotic changes in Obstructive sleep apnoea". En ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa367.

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Al-Hassi, Hafid Omar, Jonathan White, Dona Reddiar, Manel Mangalika, Dragana Cvijan, Y. Falcone, Natalie Worton et al. "PTU-014 Effects of helicobacter pylori infection on iron metabolism genes in patients with iron deficiency anaemia". En British Society of Gastroenterology, Annual General Meeting, 4–7 June 2018, Abstracts. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-bsgabstracts.282.

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Grubač, Siniša, Marko Cincović, Jože Starič, Marinković Došenović, Biljana Delić-Vujanović y Jasna Prodanov-Radulović. "The relationship of the metabolism of iron, organic matter and phlebotomy with the erythropoiesis of ruminants". En Zbornik radova 26. medunarodni kongres Mediteranske federacije za zdravlje i produkciju preživara - FeMeSPRum. Poljoprivredni fakultet Novi Sad, 2024. http://dx.doi.org/10.5937/femesprumns24012g.

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Erythropesis is the process of making red blood cells and it is related to numerous factors in the body. Iron is important because of its role in the process of making hemoglobin. In addition to the mentioned iron, it is an indirect indicator of inflammation and is regulated at the systemic and cellular level, so its lack speaks of the overall health status of individuals. Fe deficiency in the body takes place through three phases. In the first phase, there is emptying of tissue depots, but its total amount in the circulation increases, then follows the second phase or the phase of real deficit with decreasing concentration of serum iron and hemoglobin, and the third phase is the phase in which the significance of iron deficit is clinically seen. Iron deficiency disrupts all aspects of erythropoiesis. Therefore, first the iron reserves are used up, then with the decrease of transported iron, erythropoiesis changes, and when the availability of this iron is completely reduced, anemia will occur due to iron deficiency. Lipid metabolism also plays a very important role in the functioning of hematopoietic stem cells. Fatty acid oxidation is the main catabolic pathway by which energy is produced in hematopoietic stem cells. Long-chain fatty acids are activated in the cytosol and transported to the mitochondria by the transport system. In them, beta oxidation takes place through several known stages, creating acetyl coenzyme A, which starts the cycle of tricarboxylic acids. Deletion of the gene for regulation of fatty acid oxidation causes hematopoiesis stem cells to lose their potential to reconstruct and maintain themselves. Due to the importance of lipolysis in ruminants and the fact that stem cells are found in the lipidrich niches of bone marrow, we will also consider the relationship between bone marrow adipocytes and hematopoiesis. Chronic phlebotomy in rams or Fe deficiency due to inflammation and fatty liver in cows lead to specific changes in red blood cell and blood metabolites. All of the above shows that it is necessary to know the metabolic flows in order to better understand erythropoiesis in ruminants.
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Theobald, V., N. Benjamin, B. Egenlauf, H. Gall, E. Grünig, M. Halank, S. Harutyunova et al. "Association between BMPR2 mutations and iron metabolism in pulmonary arterial hypertension patients". En 61. Kongress der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e.V. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3403097.

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Paul, Bibbin, Miranda Lynch, Frank Torti y Suzy Torti. "Abstract 1501: Sideroflexin4: A novel regulator of iron metabolism in ovarian cancer". En Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1501.

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Baker, James, Christopher Mccrae, Andrew Higham, Simon Lea y Dave Singh. "Late Breaking Abstract - Neutrophilic inflammation associates with dysregulated iron metabolism in COPD." En ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa3051.

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Informes sobre el tema "Iron Metabolism"

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Kanner, Joseph, Dennis Miller, Ido Bartov, John Kinsella y Stella Harel. The Effect of Dietary Iron Level on Lipid Peroxidation of Muscle Food. United States Department of Agriculture, enero de 1995. http://dx.doi.org/10.32747/1995.7604282.bard.

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Biological oxidations are almost exclusively metal ion-promoted reactions and in ths respect iron, being the most abundant, is the commonly involved. The effect of dietary iron levels on pork, turkey and chick muscle lipid peroxidation and various other related compounds were evaluated. Crossbred feeder pigs were fed to market weight on corn-soy rations containing either 62, 131 or 209 ppm iron. After slaughter, the muscles were dissected, cooked and stored at 4°C. Heavily fortifying swine rations with iron (>200 ppm) increase nn-heme iron (NHI), thiobarbituric acid reactive substances (TBARS), and decrease a-tocopherol in cooked stored pork but did not increase warmed-over aroma (WOA). NHI and TBARS were higher in cooked pork from pigs fed high-iron diets. Liver iron correlated with muscle iron. TBARS were strongly related with WOA. The role of dietary vitamin E and ascorbic acid on Fe-induced in vivo lipid peroxidation in swine was also evaluated. Moderate elevation in iron stores had a marked effect on oxidative stress, especially as indicated by liver TBARS. Supplemental vitamin E, and to a lesser extent vitamin C, protect against this oxidative stress. Unsupplementation of Fe in the regular diet of turkeys did not affect body weight, blood hemoglobin level, or iron pool in the liver or muscle. The reason being that it contained "natural" ~120 mg Fe/kg feed, and this amount is high enough to keep constant the pool of iron in the body, liver or muscle tissues. Only Fe-supplementation with high amounts of Fe (500 ppm) significantly increased turkey blood hemoglobin and total iron in the liver, in 1 out of 3 experiments, but only slightly affects iron pool in the muscles. It seems that the liver accumulates very high concentations of iron and significantly regulates iron concentration in skeletal muscles. For this reason, it was very difficult to decrease muscle stability in turkeys through a diet containing high levels of Fe-supplementation. It was shown that the significant increase in the amount of iron (total and "free") in the muscle by injections with Fe-dextran accelerated its lipid peroxidation rate and decreased its a-tocopherol concentration. The level and metabolism of iron in the muscles affects the intensity of in vivo lipid peroxidation. This process was found to ifluence the turnover and accumulation of a-tocopherol in turkey and chick muscles. Treatments which could significantly decrease the amount and metabolism of iron pool in muscle tissues (or other organs) may affect the rate of lipid peroxidation and the turnover of a-tocopherol. Several defense enzymes were determined and found in the turkey muscle, such as superoxide dismutase, catalase, and glutathione peroxidase. Glutathione peroxidase was more active in muscles with a high trend of lipid peroxidation, lmore so in drumsticks than in breast muscles, or muscles with a low a-tocopherol content. The activity of glutathione peroxidase increased several fold in muscle stored at 4°C. Our work demonstrated that it will be much more practical to increase the stability of muscle tissues in swine, turkeys and chickens during storage and processing by increasing the amount of vitamin E in the diet than by withdrawing iron supplementation.
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2

Ades, Dennis. The role of iron nutrition in regulating patterns of photosynthesis and nitrogen metabolism in the green alga Scenedesmus quadricauda. Portland State University Library, enero de 2000. http://dx.doi.org/10.15760/etd.5533.

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Blumwald, Eduardo y Avi Sadka. Citric acid metabolism and mobilization in citrus fruit. United States Department of Agriculture, octubre de 2007. http://dx.doi.org/10.32747/2007.7587732.bard.

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Accumulation of citric acid is a major determinant of maturity and fruit quality in citrus. Many citrus varieties accumulate citric acid in concentrations that exceed market desires, reducing grower income and consumer satisfaction. Citrate is accumulated in the vacuole of the juice sac cell, a process that requires both metabolic changes and transport across cellular membranes, in particular, the mitochondrial and the vacuolar (tonoplast) membranes. Although the accumulation of citrate in the vacuoles of juice cells has been clearly demonstrated, the mechanisms for vacuolar citrate homeostasis and the components controlling citrate metabolism and transport are still unknown. Previous results in the PIs’ laboratories have indicated that the expression of a large number of a large number of proteins is enhanced during fruit development, and that the regulation of sugar and acid content in fruits is correlated with the differential expression of a large number of proteins that could play significant roles in fruit acid accumulation and/or regulation of acid content. The objectives of this proposal are: i) the characterization of transporters that mediate the transport of citrate and determine their role in uptake/retrieval in juice sac cells; ii) the study of citric acid metabolism, in particular the effect of arsenical compounds affecting citric acid levels and mobilization; and iii) the development of a citrus fruit proteomics platform to identify and characterize key processes associated with fruit development in general and sugar and acid accumulation in particular. The understanding of the cellular processes that determine the citrate content in citrus fruits will contribute to the development of tools aimed at the enhancement of citrus fruit quality. Our efforts resulted in the identification, cloning and characterization of CsCit1 (Citrus sinensis citrate transporter 1) from Navel oranges (Citrus sinesins cv Washington). Higher levels of CsCit1 transcripts were detected at later stages of fruit development that coincided with the decrease in the juice cell citrate concentrations (Shimada et al., 2006). Our functional analysis revealed that CsCit1 mediates the vacuolar efflux of citrate and that the CsCit1 operates as an electroneutral 1CitrateH2-/2H+ symporter. Our results supported the notion that it is the low permeable citrateH2 - the anion that establishes the buffer capacity of the fruit and determines its overall acidity. On the other hand, it is the more permeable form, CitrateH2-, which is being exported into the cytosol during maturation and controls the citrate catabolism in the juice cells. Our Mass-Spectrometry-based proteomics efforts (using MALDI-TOF-TOF and LC2- MS-MS) identified a large number of fruit juice sac cell proteins and established comparisons of protein synthesis patterns during fruit development. So far, we have identified over 1,500 fruit specific proteins that play roles in sugar metabolism, citric acid cycle, signaling, transport, processing, etc., and organized these proteins into 84 known biosynthetic pathways (Katz et al. 2007). This data is now being integrated in a public database and will serve as a valuable tool for the scientific community in general and fruit scientists in particular. Using molecular, biochemical and physiological approaches we have identified factors affecting the activity of aconitase, which catalyze the first step of citrate catabolism (Shlizerman et al., 2007). Iron limitation specifically reduced the activity of the cytosolic, but not the mitochondrial, aconitase, increasing the acid level in the fruit. Citramalate (a natural compound in the juice) also inhibits the activity of aconitase, and it plays a major role in acid accumulation during the first half of fruit development. On the other hand, arsenite induced increased levels of aconitase, decreasing fruit acidity. We have initiated studies aimed at the identification of the citramalate biosynthetic pathway and the role(s) of isopropylmalate synthase in this pathway. These studies, especially those involved aconitase inhibition by citramalate, are aimed at the development of tools to control fruit acidity, particularly in those cases where acid level declines below the desired threshold. Our work has significant implications both scientifically and practically and is directly aimed at the improvement of fruit quality through the improvement of existing pre- and post-harvest fruit treatments.
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Stefanova, Katya, Ginka Delcheva, Teodora Stankova, Ana Maneva, Pavel Selimov, Rositsa Karalilova y Anastas Batalov. sRANKL, OPG and sRAGE as Markers of Bone Metabolism in Rheumatoid Arthritis: Relation to Indicators of Impaired Iron Homeostasis and Inflammation. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, agosto de 2021. http://dx.doi.org/10.7546/crabs.2021.08.16.

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Splitter, Gary A., Menachem Banai y Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, enero de 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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Choudhary, Ruplal, Victor Rodov, Punit Kohli, Elena Poverenov, John Haddock y Moshe Shemesh. Antimicrobial functionalized nanoparticles for enhancing food safety and quality. United States Department of Agriculture, enero de 2013. http://dx.doi.org/10.32747/2013.7598156.bard.

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Original objectives The general goal of the project was to utilize the bactericidal potential of curcumin- functionalizednanostructures (CFN) for reinforcement of food safety by developing active antimicrobial food-contact surfaces. In order to reach the goal, the following secondary tasks were pursued: (a) further enhancement of the CFN activity based on understanding their mode of action; (b) preparing efficient antimicrobial surfaces, investigating and optimizing their performance; (c) testing the efficacy of the antimicrobial surfaces in real food trials. Background to the topic The project dealt with reducing microbial food spoilage and safety hazards. Cross-contamination through food-contact surfaces is one of the major safety concerns, aggravated by bacterial biofilm formation. The project implemented nanotech methods to develop novel antimicrobial food-contact materials based on natural compounds. Food-grade phenylpropanoidcurcumin was chosen as the most promising active principle for this research. Major conclusions, solutions, achievements In agreement with the original plan, the following research tasks were performed. Optimization of particles structure and composition. Three types of curcumin-functionalizednanostructures were developed and tested: liposome-type polydiacetylenenanovesicles, surface- stabilized nanoparticles and methyl-β-cyclodextrin inclusion complexes (MBCD). The three types had similar minimal inhibitory concentration but different mode of action. Nanovesicles and inclusion complexes were bactericidal while the nanoparticlesbacteriostatic. The difference might be due to different paths of curcumin penetration into bacterial cell. Enhancing the antimicrobial efficacy of CFN by photosensitization. Light exposure strengthened the bactericidal efficacy of curcumin-MBCD inclusion complexes approximately three-fold and enhanced the bacterial death on curcumin-coated plastic surfaces. Investigating the mode of action of CFN. Toxicoproteomic study revealed oxidative stress in curcumin-treated cells of E. coli. In the dark, this effect was alleviated by cellular adaptive responses. Under light, the enhanced ROS burst overrode the cellular adaptive mechanisms, disrupted the iron metabolism and synthesis of Fe-S clusters, eventually leading to cell death. Developing industrially-feasible methods of binding CFN to food-contact surfaces. CFN binding methods were developed for various substrates: covalent binding (binding nanovesicles to glass, plastic and metal), sonochemical impregnation (binding nanoparticles to plastics) and electrostatic layer-by-layer coating (binding inclusion complexes to glass and plastics). Investigating the performance of CFN-coated surfaces. Flexible and rigid plastic materials and glass coated with CFN demonstrated bactericidal activity towards Gram-negative (E. coli) and Gram-positive (Bac. cereus) bacteria. In addition, CFN-impregnated plastic material inhibited bacterial attachment and biofilm development. Testing the efficacy of CFN in food preservation trials. Efficient cold pasteurization of tender coconut water inoculated with E. coli and Listeriamonocytogeneswas performed by circulation through a column filled with CFN-coated glass beads. Combination of curcumin coating with blue light prevented bacterial cross contamination of fresh-cut melons through plastic surfaces contaminated with E. coli or Bac. licheniformis. Furthermore, coating of strawberries with CFN reduced fruit spoilage during simulated transportation extending the shelf life by 2-3 days. Implications, both scientific and agricultural BARD Report - Project4680 Page 2 of 17 Antimicrobial food-contact nanomaterials based on natural active principles will preserve food quality and ensure safety. Understanding mode of antimicrobial action of curcumin will allow enhancing its dark efficacy, e.g. by targeting the microbial cellular adaptation mechanisms.
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Cytryn, Eddie, Mark R. Liles y Omer Frenkel. Mining multidrug-resistant desert soil bacteria for biocontrol activity and biologically-active compounds. United States Department of Agriculture, enero de 2014. http://dx.doi.org/10.32747/2014.7598174.bard.

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Control of agro-associated pathogens is becoming increasingly difficult due to increased resistance and mounting restrictions on chemical pesticides and antibiotics. Likewise, in veterinary and human environments, there is increasing resistance of pathogens to currently available antibiotics requiring discovery of novel antibiotic compounds. These drawbacks necessitate discovery and application of microorganisms that can be used as biocontrol agents (BCAs) and the isolation of novel biologically-active compounds. This highly-synergistic one year project implemented an innovative pipeline aimed at detecting BCAs and associated biologically-active compounds, which included: (A) isolation of multidrug-resistant desert soil bacteria and root-associated bacteria from medicinal plants; (B) invitro screening of bacterial isolates against known plant, animal and human pathogens; (C) nextgeneration sequencing of isolates that displayed antagonistic activity against at least one of the model pathogens and (D) in-planta screening of promising BCAs in a model bean-Sclerotiumrolfsii system. The BCA genome data were examined for presence of: i) secondary metabolite encoding genes potentially linked to the anti-pathogenic activity of the isolates; and ii) rhizosphere competence-associated genes, associated with the capacity of microorganisms to successfully inhabit plant roots, and a prerequisite for the success of a soil amended BCA. Altogether, 56 phylogenetically-diverse isolates with bioactivity against bacterial, oomycete and fungal plant pathogens were identified. These strains were sent to Auburn University where bioassays against a panel of animal and human pathogens (including multi-drug resistant pathogenic strains such as A. baumannii 3806) were conducted. Nineteen isolates that showed substantial antagonistic activity against at least one of the screened pathogens were sequenced, assembled and subjected to bioinformatics analyses aimed at identifying secondary metabolite-encoding and rhizosphere competence-associated genes. The genome size of the bacteria ranged from 3.77 to 9.85 Mbp. All of the genomes were characterized by a plethora of secondary metabolite encoding genes including non-ribosomal peptide synthase, polyketidesynthases, lantipeptides, bacteriocins, terpenes and siderophores. While some of these genes were highly similar to documented genes, many were unique and therefore may encode for novel antagonistic compounds. Comparative genomic analysis of root-associated isolates with similar strains not isolated from root environments revealed genes encoding for several rhizospherecompetence- associated traits including urea utilization, chitin degradation, plant cell polymerdegradation, biofilm formation, mechanisms for iron, phosphorus and sulfur acquisition and antibiotic resistance. Our labs are currently writing a continuation of this feasibility study that proposes a unique pipeline for the detection of BCAs and biopesticides that can be used against phytopathogens. It will combine i) metabolomic screening of strains from our collection that contain unique secondary metabolite-encoding genes, in order to isolate novel antimicrobial compounds; ii) model plant-based experiments to assess the antagonistic capacities of selected BCAs toward selected phytopathogens; and iii) an innovative next-generation-sequencing based method to monitor the relative abundance and distribution of selected BCAs in field experiments in order to assess their persistence in natural agro-environments. We believe that this integrated approach will enable development of novel strains and compounds that can be used in large-scale operations.
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