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[PMID]:28465342
[Au] Autor:Stefanova D; Raychev A; Arezes J; Ruchala P; Gabayan V; Skurnik M; Dillon BJ; Horwitz MA; Ganz T; Bulut Y; Nemeth E
[Ad] Endereço:Molecular, Cellular, and Integrative Physiology Graduate Program and.
[Ti] Título:Endogenous hepcidin and its agonist mediate resistance to selected infections by clearing non-transferrin-bound iron.
[So] Source:Blood;130(3):245-257, 2017 07 20.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The iron-regulatory hormone hepcidin is induced early in infection, causing iron sequestration in macrophages and decreased plasma iron; this is proposed to limit the replication of extracellular microbes, but could also promote infection with macrophage-tropic pathogens. The mechanisms by which hepcidin and hypoferremia modulate host defense, and the spectrum of microbes affected, are poorly understood. Using mouse models, we show that hepcidin was selectively protective against siderophilic extracellular pathogens ( O9) by controlling non-transferrin-bound iron (NTBI) rather than iron-transferrin concentration. NTBI promoted the rapid growth of siderophilic but not nonsiderophilic bacteria in mice with either genetic or iatrogenic iron overload and in human plasma. Hepcidin or iron loading did not affect other key components of innate immunity, did not indiscriminately promote intracellular infections ( ), and had no effect on extracellular nonsiderophilic O8 or Hepcidin analogs may be useful for treatment of siderophilic infections.
[Mh] Termos MeSH primário: Infecções Relacionadas a Cateter/imunologia
Hemocromatose/imunologia
Hepcidinas/imunologia
Sobrecarga de Ferro/imunologia
Ferro/metabolismo
Infecções Estafilocócicas/imunologia
[Mh] Termos MeSH secundário: Animais
Ligação Competitiva
Infecções Relacionadas a Cateter/metabolismo
Infecções Relacionadas a Cateter/microbiologia
Infecções Relacionadas a Cateter/mortalidade
Modelos Animais de Doenças
Resistência à Doença
Expressão Gênica
Hemocromatose/metabolismo
Hemocromatose/microbiologia
Hemocromatose/mortalidade
Hepcidinas/agonistas
Hepcidinas/deficiência
Hepcidinas/genética
Seres Humanos
Ferro/imunologia
Sobrecarga de Ferro/metabolismo
Sobrecarga de Ferro/microbiologia
Sobrecarga de Ferro/mortalidade
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mycobacterium tuberculosis/efeitos dos fármacos
Mycobacterium tuberculosis/crescimento & desenvolvimento
Mycobacterium tuberculosis/metabolismo
Oligopeptídeos/farmacologia
Ligação Proteica
Infecções Estafilocócicas/metabolismo
Infecções Estafilocócicas/microbiologia
Infecções Estafilocócicas/mortalidade
Staphylococcus aureus
Análise de Sobrevida
Transferrina/genética
Transferrina/metabolismo
Yersinia enterocolitica/efeitos dos fármacos
Yersinia enterocolitica/crescimento & desenvolvimento
Yersinia enterocolitica/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hamp1 protein, mouse); 0 (Hepcidins); 0 (Oligopeptides); 0 (Transferrin); E1UOL152H7 (Iron)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-03-772715


  2 / 15758 MEDLINE  
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[PMID]:29275107
[Au] Autor:Moghimipour E; Rezaei M; Ramezani Z; Kouchak M; Amini M; Angali KA; Dorkoosh FA; Handali S
[Ad] Endereço:Nanotechnology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Cellular and Molecular Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
[Ti] Título:Transferrin targeted liposomal 5-fluorouracil induced apoptosis via mitochondria signaling pathway in cancer cells.
[So] Source:Life Sci;194:104-110, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to prepare transferrin (Tf) targeted liposomal 5-Fluorouracil (5FU) to improve the safety and efficacy of the drug. Liposomes were prepared using thin layer method. Morphology of liposomes was characterized by transmission electron microscopy (TEM) and their particle size was also determined. The in vitro cytotoxicity was investigated via MTT assay on HT-29 (as cancer cell) and fibroblast (as normal cell). Moreover, cytotoxicity mechanism of targeted liposomes was determined through the production of reactive oxygen species (ROS), mitochondrial membrane potential (∆Ψ ) and release of cytochrome c. Results showed that encapsulation efficiency (EE%) was 58.66±0.58 and average size of liposomes was 107nm. Also, nano-particles were spherical as shown by TEM. MTT assay on HT-29 cells revealed the higher cytotoxic activity of targeted liposomes in comparison to free drug and non-targeted liposome. In contrast, comparing with cancer cells, targeted liposomes had no cytotoxic effect on normal cells. In addition, targeted liposomes induced apoptosis through activation of mitochondrial apoptosis pathways, as evidenced by decreased mitochondrial membrane potential and release of cytochrome c. Results of the study indicated that targeted liposomes would provide a potential strategy to treat colon cancer by inducing apoptosis via mitochondria signaling pathway with reducing dose of the drug and resulting fewer side-effects.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Neoplasias do Colo/tratamento farmacológico
Fluoruracila/farmacologia
Transdução de Sinais/efeitos dos fármacos
Transferrina/metabolismo
[Mh] Termos MeSH secundário: Antimetabólitos Antineoplásicos/administração & dosagem
Linhagem Celular
Neoplasias do Colo/metabolismo
Sistemas de Liberação de Medicamentos
Fluoruracila/administração & dosagem
Células HT29
Seres Humanos
Lipossomos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Liposomes); 0 (Reactive Oxygen Species); 0 (Transferrin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171225
[St] Status:MEDLINE


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[PMID]:28466468
[Au] Autor:Brown FC; Collett M; Tremblay CS; Rank G; De Camilli P; Booth CJ; Bitoun M; Robinson PJ; Kile BT; Jane SM; Curtis DJ
[Ad] Endereço:Australian Centre for Blood Diseases, Central Clinical School, Monash University and Alfred Health, Melbourne, Vic., Australia.
[Ti] Título:Loss of Dynamin 2 GTPase function results in microcytic anaemia.
[So] Source:Br J Haematol;178(4):616-628, 2017 08.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In a dominant mouse ethylnitrosurea mutagenesis screen for genes regulating erythropoiesis, we identified a pedigree with a novel microcytic hypochromia caused by a V235G missense mutation in Dynamin 2 (Dnm2). Mutations in Dnm2, a GTPase, are highly disease-specific and have been implicated in four forms of human diseases: centronuclear myopathy, Charcot-Marie Tooth neuropathy and, more recently, T-cell leukaemia and Hereditary Spastic Paraplegia, but red cell abnormalities have not been reported to date. The V235G mutation lies within a crucial GTP nucleotide-binding pocket of Dnm2, and resulted in defective GTPase activity and incompatibility with life in the homozygous state. Dnm2 is an essential mediator of clathrin-mediated endocytosis, which is required for the uptake of transferrin (Tf) into red cells for incorporation of haem. Accordingly, we observed significantly reduced Tf uptake by Dnm2 cells, which led to impaired endosome formation. Despite these deficiencies, surprisingly all iron studies were unchanged, suggesting an unexplained alternative mechanism underlies microcytic anaemia in Dnm2 mice. This study provides the first in vivo evidence for the requirements of Dnm2 in normal erythropoiesis.
[Mh] Termos MeSH primário: Anemia Hipocrômica/genética
Dinamina II/genética
Mutação de Sentido Incorreto
[Mh] Termos MeSH secundário: Anemia Hipocrômica/sangue
Animais
Mapeamento Cromossômico/métodos
Modelos Animais de Doenças
Dinamina II/deficiência
Dinamina II/fisiologia
Endocitose/genética
Endocitose/fisiologia
Eritrócitos/metabolismo
Eritrócitos/patologia
Genótipo
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Camundongos Knockout
Transferrina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Transferrin); EC 3.6.5.5 (Dynamin II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14709


  4 / 15758 MEDLINE  
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[PMID]:29176318
[Au] Autor:Tang Y; Jia W; Niu X; Wu L; Shen H; Wang L; Qi R; Ling C; Li M
[Ad] Endereço:Military Hygiene Department, Faculty of Naval Medicine, Second Military Medical University, Shanghai, China.
[Ti] Título:CCL2 is Upregulated by Decreased miR-122 Expression in Iron-Overload-Induced Hepatic Inflammation.
[So] Source:Cell Physiol Biochem;44(3):870-883, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Iron overload (IO) is accompanied by hepatic inflammation. The chemokine (C-C motif) ligand 2 (CCL2) mediates inflammation, and its overexpression is associated with IO. However, whether IO results in CCL2 overexpression in the liver and the underlying mechanisms are unclear. METHODS: We subjected mice to IO by administering intraperitoneal injections of dextran-iron or by feeding mice a 3% dextran-iron diet to observe the effects of IO on miR-122/CCL2 expression through real-time qPCR and Western blot analysis. We also used indicators, including the expression of the inflammatory cytokine, the inflammation score based on H&E staining and the serum content of ALT and AST to evaluate the effects of IO on hepatic inflammation. Meanwhile, we observed the effects of vitamin E on IO-induced hepatic inflammation. In cells, we used 100 µΜ FeSO4 or 30 µΜ Holo-Tf to produce IO and observed the roles of miR-122 in regulating CCL2 expression by using miR-122 mimics or inhibitors to overexpress or inhibit miR-122. Then, we used a dual-luciferase reporter assay to prove that miR-122 regulates CCL2 expression through direct binding to its complementary sequence in the CCL2 mRNA 3'UTR. RESULTS: IO induces the downregulation of miR-122 and the upregulation of CCL2, as well as inflammatory responses both in vitro and in vivo. Although IO-induced oxidative stress is eliminated by the antioxidant vitamin E, IO-induced hepatic inflammation still exists, which probably can be explained by the fact that vitamin E has no effects on the miR-122/CCL2 pathway. In in vitro experiments, the overexpression and inhibition of miR-122 significantly reduced and increased CCL2 expression, respectively. The dual-luciferase reporter assay indicates that miR-122 binds CCL2 mRNA 3'UTR. CONCLUSION: We propose the roles of miR-122/CCL2 in IO-induced hepatic inflammation. Our studies should provide a new clue for developing clinical strategies for patients with IO.
[Mh] Termos MeSH primário: Quimiocina CCL2/metabolismo
Complexo Ferro-Dextran/toxicidade
Fígado/patologia
MicroRNAs/metabolismo
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Antagomirs/metabolismo
Sequência de Bases
Linhagem Celular
Quimiocina CCL2/antagonistas & inibidores
Quimiocina CCL2/genética
Compostos Ferrosos/toxicidade
Seres Humanos
Inflamação
Interleucina-6/sangue
Ferro/análise
Ferro/sangue
Fígado/efeitos dos fármacos
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Estresse Oxidativo/efeitos dos fármacos
Alinhamento de Sequência
Fator de Transcrição RelA/genética
Fator de Transcrição RelA/metabolismo
Transferrina/farmacologia
Fator de Necrose Tumoral alfa/sangue
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Vitamina E/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (Chemokine CCL2); 0 (Ferrous Compounds); 0 (Interleukin-6); 0 (MicroRNAs); 0 (Mirn122 microRNA, mouse); 0 (Transcription Factor RelA); 0 (Transferrin); 0 (Tumor Necrosis Factor-alpha); 1406-18-4 (Vitamin E); 39R4TAN1VT (ferrous sulfate); 9004-66-4 (Iron-Dextran Complex); E1UOL152H7 (Iron)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485355


  5 / 15758 MEDLINE  
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[PMID]:29227592
[Au] Autor:Chekhun VF; Lozovska YV; Burlaka AP; Ganusevich LI; Shvets YV; Lukyanova NY; Todor IM; Tregubova NA; Naleskina LA
[Ti] Título:Remodulating effect of doxorubicin on the state of iron-containing proteins, and redox characteristics of tumor with allowance for its sensitivity to cytostatic agents.
[So] Source:Ukr Biochem J;88(1):99-108, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The study was aimed at determining the changes of metal-containing proteins in blood serum and tumor tissue of animals with parental and doxorubicin-resistant strains of Walker-256 carcinosarcoma before and after the cytostatic administration. It has been shown that upon doxorubicin action the levels of total iron and transferrin in the tissues from the both groups of animals decreased while that of ferritine simultaneously increased with more pronounced pattern in the group of animals with resistant tumor strain. It has been shown that upon the action of doxorubicin in tumor tissue of animals with different sensitivity to the cytostatic there could be observed oppositely directed changes in the redox state of these cells that in turn determined the content of " free iron" complexes, RO S generation and concentration of active forms of matrix metaloproteinase- 2 and matrix metaloproteinase-9, namely, the increase of these indexes in animals with parental strain and their decrease in animals with the resistant one. So, our study has demonstrated the remodulating effect of doxorubicin on the state of metal-containing proteins and redox characteristics of tumor dependent on its sensitivity to cytostatic, at the levels of the tumor and an organism. These data may serve as a criterion for the development of programs for the correction of malfunction of iron metabolism aimed at elevating tumor sensitivity to cytostatic agents.
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/farmacologia
Carcinoma 256 de Walker/tratamento farmacológico
Doxorrubicina/farmacologia
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Ferro/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma 256 de Walker/genética
Carcinoma 256 de Walker/metabolismo
Carcinoma 256 de Walker/patologia
Resistência a Medicamentos Antineoplásicos/genética
Feminino
Ferritinas/genética
Ferritinas/metabolismo
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Transplante de Neoplasias
Ratos
Ratos Endogâmicos
Espécies Reativas de Oxigênio/metabolismo
Transferrina/genética
Transferrina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Reactive Oxygen Species); 0 (Transferrin); 80168379AG (Doxorubicin); 9007-73-2 (Ferritins); E1UOL152H7 (Iron); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, rat); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, rat)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.099


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[PMID]:28457853
[Au] Autor:Bruneel A; Habarou F; Stojkovic T; Plouviez G; Bougas L; Guillemet F; Brient N; Henry D; Dupré T; Vuillaumier-Barrot S; Seta N
[Ad] Endereço:AP-HP, Biochimie Métabolique et Cellulaire, Hôpital Bichat, Paris, France; INSERM UMR-1193 "Mécanismes cellulaires et moléculaires de l'adaptation au stress et cancérogenèse", Université Paris-Sud, Châtenay-Malabry, France; Université Paris-Sud, France. Electronic address: arnaud.bruneel@aphp.fr.
[Ti] Título:Two-dimensional electrophoresis highlights haptoglobin beta chain as an additional biomarker of congenital disorders of glycosylation.
[So] Source:Clin Chim Acta;470:70-74, 2017 Jul.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Congenital disorders of glycosylation (CDGs) are rare inherited disorders affecting glycosylation of proteins and lipids and sharing very heterogeneous multivisceral symptoms. The biochemical screening of these diseases is currently limited to electrophoresis or HPLC separation/quantification of serum transferrin glycoforms and is relatively frequently hampered by genetic polymorphism. Further, it has been shown that transferrin glycosylation can be very poorly affected in confirmed CDGs. We developed a fast and simple two-dimensional (2-DE) Western-blot analysis applied to the simultaneous detection of various serum glycoproteins, i.e. haptoglobin, α1-anti-trypsin, transferrin and α1-acid glycoprotein, and applied it to a large cohort of CDGs and secondary glycosylation disorders. When separated using 2-DE, haptoglobin ß glycoforms showed clear abnormalities in all interpretable CDG type I and CDG type II patterns. Although secondary glycosylation defects such as alcoholism, untreated fructosemia and bacterial neuraminidase remain to be excluded, we showed that 2-DE pattern of haptoglobin ß glycoforms thus constitute a very reliable additional biomarker of all types of CDGs. Coupled with common screening techniques and glycans mass spectrometry, it can orientate and facilitate the way towards CDG molecular diagnostic.
[Mh] Termos MeSH primário: Defeitos Congênitos da Glicosilação/metabolismo
Eletroforese em Gel Bidimensional
Haptoglobinas/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Glicosilação
Haptoglobinas/isolamento & purificação
Seres Humanos
Transferrina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Haptoglobins); 0 (Transferrin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  7 / 15758 MEDLINE  
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[PMID]:29054412
[Au] Autor:Duck KA; Simpson IA; Connor JR
[Ad] Endereço:Department of Neurosurgery, Penn State Hershey Medical Center, Hershey, PA, United States.
[Ti] Título:Regulatory mechanisms for iron transport across the blood-brain barrier.
[So] Source:Biochem Biophys Res Commun;494(1-2):70-75, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many critical metabolic functions in the brain require adequate and timely delivery of iron. However, most studies when considering brain iron uptake have ignored the iron requirements of the endothelial cells that form the blood-brain barrier (BBB). Moreover, current models of BBB iron transport do not address regional regulation of brain iron uptake or how neurons, when adapting to metabolic demands, can acquire more iron. In this study, we demonstrate that both iron-poor transferrin (apo-Tf) and the iron chelator, deferoxamine, stimulate release of iron from iron-loaded endothelial cells in an in vitro BBB model. The role of the endosomal divalent metal transporter 1 (DMT1) in BBB iron acquisition and transport has been questioned. Here, we show that inhibition of DMT1 alters the transport of iron and Tf across the endothelial cells. These data support an endosome-mediated model of Tf-bound iron uptake into the brain and identifies mechanisms for local regional regulation of brain iron uptake. Moreover, our data provide an explanation for the disparity in the ratio of Tf to iron transport into the brain that has confounded the field.
[Mh] Termos MeSH primário: Barreira Hematoencefálica/metabolismo
Ferro/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico Ativo/efeitos dos fármacos
Barreira Hematoencefálica/efeitos dos fármacos
Encéfalo/irrigação sanguínea
Encéfalo/metabolismo
Proteínas de Transporte de Cátions/antagonistas & inibidores
Proteínas de Transporte de Cátions/metabolismo
Bovinos
Células Cultivadas
Endossomos/metabolismo
Células Endoteliais/metabolismo
Hepcidinas/metabolismo
Microvasos/metabolismo
Modelos Neurológicos
Transferrina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cation Transport Proteins); 0 (Hepcidins); 0 (Transferrin); 0 (solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2); E1UOL152H7 (Iron)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171022
[St] Status:MEDLINE


  8 / 15758 MEDLINE  
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[PMID]:28988537
[Au] Autor:Sokolov AV; Voynova IV; Kostevich VA; Vlasenko AY; Zakharova ET; Vasilyev VB
[Ad] Endereço:Institute of Experimental Medicine, St. Petersburg, 197376, Russia. biochemsokolov@gmail.com.
[Ti] Título:Comparison of Interaction between Ceruloplasmin and Lactoferrin/Transferrin: to Bind or Not to Bind.
[So] Source:Biochemistry (Mosc);82(9):1073-1078, 2017 Sep.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The year 2016 marked the 50th anniversary of the discovery by S. Osaki who first showed that ceruloplasmin (CP, ferro:O -oxidoreductase or ferroxidase) is capable of oxidizing Fe(II) to Fe(III) and favors the incorporation of the latter into transferrin (TF). However, much debate remains in the literature concerning the existence of a complex between the enzyme oxidizing iron and the protein facilitating its transport in plasma. We studied CP in exocrine fluids and demonstrated its high-affinity interaction with transferrin found in breast milk and in lacrimal fluid, i.e. with lactoferrin (LF). Here we present data obtained by comparing the interaction of CP with LF and TF using surface plasmon resonance and Hummel-Dreyer chromatography. Binding of apo-LF within the range of concentrations 1.6-51.3 µM with CP immobilized on a CM5-chip is characterized by K = 1.07 µM. Under similar conditions, the K for apo-TF was measured and appeared to be higher than 51.3 µM. Hummel-Dreyer chromatography of CP with 51 µM apo-LF/apo-TF in the effluent demonstrated the absence of interaction between apo-TF and CP in solution, contrary to efficient interaction between apo-LF and CP. In contrast to LF, the interaction of apo-TF with CP is probably not stable within the physiological range of concentrations of TF.
[Mh] Termos MeSH primário: Ceruloplasmina/metabolismo
Lactoferrina/metabolismo
Leite Humano/química
Lágrimas/química
Transferrina/metabolismo
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Leite Humano/metabolismo
Ligação Proteica
Lágrimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Transferrin); EC 1.16.3.1 (Ceruloplasmin); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917090115


  9 / 15758 MEDLINE  
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[PMID]:28935588
[Au] Autor:Kindrat I; Dreval K; Shpyleva S; Tryndyak V; de Conti A; Mudalige TK; Chen T; Erstenyuk AM; Beland FA; Pogribny IP
[Ad] Endereço:Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, AR, 72079, United States; Department of Biological and Medical Chemistry, Ivano-Frankivsk National Medical University, Ivano-Frankivsk, Ukraine.
[Ti] Título:Effect of methapyrilene hydrochloride on hepatic intracellular iron metabolism in vivo and in vitro.
[So] Source:Toxicol Lett;281:65-73, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The liver, a central detoxification organ and main regulator of systemic iron homeostasis, is prone to damage by xenobiotics. In the present study, we investigated the effect of the hepatotoxicant and hepatocarcinogen methapyrilene hydrochloride on iron metabolism in rat liver in a repeat-dose in vivo toxicity study and in human HepaRG cells in vitro. Treatment of male Fischer 344 (F344) rats with methapyrilene at doses 40 and 80mg/kg body weight (bw)/day by gavage for 6 weeks resulted in changes in the expression of classic hepatotoxicity-related marker genes and iron homeostasis-related genes, especially a prominent, dose-dependent down-regulation of the transferrin (Tf) gene and an up-regulation of the ferritin, light chain (Ftl) gene. A decrease in the level of TF and an increase in the level of FTL also occurred in methapyrilene-treated differentiated HepaRG cells, indicating the existence of interspecies and in vitro-in vivo similarities in the disturbance of cellular iron homeostasis upon liver injury. In contrast, there was minimal overlap in the expression of liver toxicity-marker genes in the livers of rats and in HepaRG cells treated with methapyrilene. Importantly, the decrease of transferrin at mRNA and protein levels occurred after the treatment with a low dose of methapyrilene that exhibited minimal cytotoxicity. These results demonstrate the significance of the dysregulation of hepatic iron metabolism in the pathogenesis and mechanism of chemical-induced liver toxicity and suggest that these changes may be sensitive and useful indicators of potentially hepatotoxic chemicals.
[Mh] Termos MeSH primário: Ferro/metabolismo
Fígado/efeitos dos fármacos
Metapirileno/toxicidade
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Relação Dose-Resposta a Droga
Regulação para Baixo
Ferritinas/genética
Ferritinas/metabolismo
Marcadores Genéticos
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Fígado/metabolismo
Masculino
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Endogâmicos F344
Transferrina/genética
Transferrina/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Genetic Markers); 0 (RNA, Messenger); 0 (Transferrin); 9007-73-2 (Ferritins); A01LX40298 (Methapyrilene); E1UOL152H7 (Iron)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE


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[PMID]:28870956
[Au] Autor:Bi YE; Zhou Y; Wang M; Li L; Lee RJ; Xie J; Teng L
[Ad] Endereço:Jilin University, College of Life Science, P. R. China.
[Ti] Título:Targeted Delivery of Cordycepin to Liver Cancer Cells Using Transferrin-conjugated Liposomes.
[So] Source:Anticancer Res;37(9):5207-5214, 2017 09.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Cordycepin is an endogenous nucleoside with significant anticancer biological activity. The objective of this study was to develop targeted liposomes to improve solubility and biological activity of cordycepin. MATERIALS AND METHODS: We established transferrin-conjugated liposomes to deliver cordycepin to liver cancer cells and evaluated the uptake and effect. RESULTS: The liposomes were loaded with cordycepin. Their average size was 125.3 nm, with drug encapsulation efficiency of 65.3%. The liposomes had good colloidal stability and released cordycepin slowly. Liposomal cordycepin was shown to increase reactive oxygen species production and cause depolarization of the mitochondrial transmembrane in liver cancer cells. Cellular uptake of liposomal cordycepin was enhanced by conjugation to transferrin, that facilitated receptor-mediated endocytosis. CONCLUSION: Transferrin-conjugated liposomes are effective as nanocarriers for cordycepin delivery to liver cancer cells.
[Mh] Termos MeSH primário: Desoxiadenosinas/uso terapêutico
Sistemas de Liberação de Medicamentos
Neoplasias Hepáticas/tratamento farmacológico
Transferrina/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Desoxiadenosinas/farmacologia
Fluorescência
Seres Humanos
Lipossomos
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/ultraestrutura
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Tamanho da Partícula
Espécies Reativas de Oxigênio/metabolismo
Eletricidade Estática
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Deoxyadenosines); 0 (Liposomes); 0 (Reactive Oxygen Species); 0 (Transferrin); GZ8VF4M2J8 (cordycepin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE



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