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[PMID]:28460441
[Au] Autor:Arora J; Sauer SJ; Tarpley M; Vermeulen P; Rypens C; Van Laere S; Williams KP; Devi GR; Dewhirst MW
[Ad] Endereço:Duke Cancer Institute, Duke University, Durham, NC, USA.
[Ti] Título:Inflammatory breast cancer tumor emboli express high levels of anti-apoptotic proteins: use of a quantitative high content and high-throughput 3D IBC spheroid assay to identify targeting strategies.
[So] Source:Oncotarget;8(16):25848-25863, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory breast cancer (IBC) is one of the most lethal breast cancer variants; with existing therapy, 5-yr survival rate is only 35%. Current barriers to successful treatment of IBC include frequent infiltration and the presence of tumor cell clusters, termed tumor emboli, within the breast parenchyma and lymphatics. Prior studies have identified the role of anti-apoptotic signaling, in particular hyperactivation of NFκB and its target genes, in IBC pathobiology and therapeutic resistance. The objectives of this study were to: (1) determine if IBC tumor emboli express anti-apoptotic proteins and (2) develop a high content, multiparametric assay to assess the morphology of the IBC 3D spheroids and to optimize a high throughput format to screen for compounds that can inhibit the formation of the IBC tumor clusters/embolic structures. Immunohistochemical analysis of IBC patient tumor samples with documented tumor emboli revealed high NFκB (p65) staining along with expression of XIAP, a potent anti-apoptotic protein known to interact with NFκB signaling in enhancing survival of malignant cells. Subsequently, the high content assay developed allowed for simultaneous imaging and morphometric analysis, including count and viability of spheroids derived from SUM149, rSUM149 and SUM190 cells and its application to evaluate XIAP and NFκB inhibitory agents. We demonstrate the efficacy of the off-patent drug disulfiram when chelated with copper, which we had previously reported to inhibit NFκB signaling, was highly effective in disrupting both IBC spheroids and emboli grown in vitro. Taken together, these results identify a high-throughput approach to target tumor spheroid formation for drug discovery. Finally, disulfiram is a safe and approved drug for management of alcohol abuse, warranting its evaluation for repurposing in IBC therapy.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/genética
Neoplasias Inflamatórias Mamárias/genética
Neoplasias Inflamatórias Mamárias/patologia
Células Neoplásicas Circulantes/metabolismo
[Mh] Termos MeSH secundário: Proteínas Reguladoras de Apoptose/metabolismo
Biomarcadores Tumorais
Técnicas de Cultura de Células
Sobrevivência Celular/genética
Cobre/farmacologia
Dissulfiram/farmacologia
Feminino
Expressão Gênica
Ensaios de Triagem em Larga Escala
Seres Humanos
Neoplasias Inflamatórias Mamárias/metabolismo
Mitocôndrias/metabolismo
NF-kappa B/genética
NF-kappa B/metabolismo
Esferoides Celulares
Células Tumorais Cultivadas
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/genética
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Biomarkers, Tumor); 0 (NF-kappa B); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 789U1901C5 (Copper); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15667


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[PMID]:29227611
[Au] Autor:Rushchak VV; Chashchyn MO
[Ti] Título:Cytochrome P450 2E1 participation in the pathogenesis of experimental metabolic syndrome in guinea pigs.
[So] Source:Ukr Biochem J;88(2):98-106, 2016 Mar-Apr.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:In this work the experimental metabolic syndrome on the basis of protamine sulfate modeling in guinea pigs was reproduced and pathological processes in the liver of experimental animals were studied. We determined the level of free radicals and markers of liver damage in the blood of experimental animals. We investigated the liver glycogen content and K+,Na+-ATPase activity in the liver of experimental animals as well as measured the cytochrome P450 2E1 (CY P2E1) expression ­ one of the main factors of oxidative stress. Evidence of development of hepatotoxic processes, increasing of the CY P2E1 level as well as of the free radical level in the animals with metabolic syndrome were found. Using of CY P2E1 inhibitors had shown that the free radical level in the blood of experimental animals depended on the level of the enzyme expression and activity. The obtained results suggest that the changes in the CY P2E1 expression play an important role in the development of hepatotoxic processes upon experimental metabolic syndrome. It was assumed that pharmacological correction of the enzyme expression may be an important mechanism for the influence on the metabolic syndrome clinical course.
[Mh] Termos MeSH primário: Inibidores do Citocromo P-450 CYP2E1/farmacologia
Citocromo P-450 CYP2E1/genética
Fígado/efeitos dos fármacos
Síndrome Metabólica/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Citocromo P-450 CYP2E1/metabolismo
Dissulfiram/farmacologia
Radicais Livres/antagonistas & inibidores
Radicais Livres/metabolismo
Regulação da Expressão Gênica
Glicogênio/metabolismo
Cobaias
Fígado/enzimologia
Fígado/patologia
Masculino
Síndrome Metabólica/induzido quimicamente
Síndrome Metabólica/enzimologia
Síndrome Metabólica/patologia
Estresse Oxidativo/efeitos dos fármacos
Protaminas
Pirazóis/farmacologia
Quercetina/farmacologia
ATPase Trocadora de Sódio-Potássio/genética
ATPase Trocadora de Sódio-Potássio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytochrome P-450 CYP2E1 Inhibitors); 0 (Free Radicals); 0 (Protamines); 0 (Pyrazoles); 83LCM6L2BY (fomepizole); 9005-79-2 (Glycogen); 9IKM0I5T1E (Quercetin); EC 1.14.13.- (Cytochrome P-450 CYP2E1); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); TR3MLJ1UAI (Disulfiram)
[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/ubj88.02.098


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[PMID]:28887129
[Au] Autor:Hasinoff BB; Patel D
[Ad] Endereço:College of Pharmacy, Apotex Centre, University of Manitoba, Winnipeg, Manitoba R3E 0T5, Canada. Electronic address: B_Hasinoff@UManitoba.ca.
[Ti] Título:Disulfiram is a slow-binding partial noncompetitive inhibitor of 20S proteasome activity.
[So] Source:Arch Biochem Biophys;633:23-28, 2017 Nov 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The alcohol abuse drug disulfiram has also been shown to exhibit potent cell growth inhibitory and anticancer activity. While a number of cellular and animal studies have suggested that disulfiram exhibits its anticancer activity through interaction with the proteasome, direct evidence for inhibition of proteasome activity is lacking. In this study we show that disulfiram potently inhibits the chymotrypsin-like activity of purified human 20S proteasome at low micromolar pharmacological concentrations. The enzyme progress curves displayed characteristics of a slow-binding reaction, similar to that observed for the FDA-approved proteasomal-targeted anticancer drugs bortezomib and carfilzomib. The apparent second order rate constant for reaction with 20s proteasome that was derived from an analysis of the progress curves was about 250-fold smaller than for bortezomib and carfilzomib. The concentration dependence of the enzyme kinetics was consistent with partial noncompetitive inhibition, whereby the putative disulfiram-proteasome adduct retains, partial but decreased enzyme activity. Disulfiram, which is known to have a high affinity for protein thiols, likely reacted with a non-critical cysteine residue, and not at the proteasome substrate binding site.
[Mh] Termos MeSH primário: Inibidores de Acetaldeído Desidrogenases/farmacologia
Dissulfiram/farmacologia
Complexo de Endopeptidases do Proteassoma/efeitos dos fármacos
Inibidores de Proteassoma/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Bortezomib/farmacologia
Sistema Livre de Células/efeitos dos fármacos
Sistema Livre de Células/enzimologia
Seres Humanos
Cinética
Oligopeptídeos/farmacologia
Complexo de Endopeptidases do Proteassoma/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetaldehyde Dehydrogenase Inhibitors); 0 (Antineoplastic Agents); 0 (Oligopeptides); 0 (Proteasome Inhibitors); 69G8BD63PP (Bortezomib); 72X6E3J5AR (carfilzomib); EC 3.4.25.1 (Proteasome Endopeptidase Complex); TR3MLJ1UAI (Disulfiram)
[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:170910
[St] Status:MEDLINE


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[PMID]:28864067
[Au] Autor:Cong J; Wang Y; Zhang X; Zhang N; Liu L; Soukup K; Michelakos T; Hong T; DeLeo A; Cai L; Sabbatino F; Ferrone S; Lee H; Levina V; Fuchs B; Tanabe K; Lillemoe K; Ferrone C; Wang X
[Ad] Endereço:Division of Surgical Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
[Ti] Título:A novel chemoradiation targeting stem and nonstem pancreatic cancer cells by repurposing disulfiram.
[So] Source:Cancer Lett;409:9-19, 2017 Nov 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Pancreatic ductal adenocarcinoma (PDAC) has a 5-year relative survival rate of 8% and is projected to be the second leading cause of cancer death by 2030, underscoring the urgency to develop new strategies to improve current therapeutic modalities for PDAC. Targeting pancreatic cancer stem cells (PCSCs), which are resistant to radiation and chemotherapy, is a promising strategy. A novel approach which can be readily clinically translated is to repurpose disulfiram (DSF), a drug for treating alcoholism, to target PCSCs. Chemoradiation or the combination of chemotherapy agents FOLFIRINOX, currently standard care for PDAC, can increase stemness in some established or primary PDAC cell lines. However, DSF in the presence of exogenously or endogenously supplied copper (Cu), when combined with chemotherapy or chemoradiation, targets both PCSCs and nonstem PDAC cells. Previously, we demonstrated that DSF/Cu effectively targets breast cancer stem cells in the context of fractionated radiation (FIR) by inhibiting the NF-κB-stemness gene pathway. Therefore, the hypothesis that PCSCs can be effectively targeted by incorporating DSF/Cu into the standard chemoradiation regimen consisting of 5-FU and FIR was investigated and found to be effective in vitro in targeting PCSCs, identified as either ALDH or CD24+/CD44+/ESA+ or sphere-forming cells, as well as nonstem PDAC cells. In vivo, the combination of IR+5-FU+DSF/Cu was more effective (72.46%) than either IR+5-FU (30.32%) or IR+FOLFIRINOX therapy (43.04%) in inhibiting growth of the mouse Panc02 tumor. These encouraging results provide a solid foundation for clinical trials to improve the outcomes of the current standard chemoradiation therapy regimen for PDAC.
[Mh] Termos MeSH primário: Carcinoma Ductal Pancreático/tratamento farmacológico
Carcinoma Ductal Pancreático/radioterapia
Dissulfiram/farmacologia
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/efeitos da radiação
Neoplasias Pancreáticas/tratamento farmacológico
Neoplasias Pancreáticas/radioterapia
[Mh] Termos MeSH secundário: Inibidores de Acetaldeído Desidrogenases/farmacologia
Animais
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/patologia
Linhagem Celular Tumoral
Quimiorradioterapia
Cobre/farmacologia
Reposicionamento de Medicamentos
Feminino
Fluoruracila/farmacologia
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Células-Tronco Neoplásicas/patologia
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
Radiossensibilizantes/farmacologia
Distribuição Aleatória
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetaldehyde Dehydrogenase Inhibitors); 0 (Radiation-Sensitizing Agents); 789U1901C5 (Copper); C955P95064 (cuprous chloride); TR3MLJ1UAI (Disulfiram); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE


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[PMID]:28768860
[Au] Autor:Chen SC; Jeng KS; Lai MMC
[Ad] Endereço:Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan.
[Ti] Título:Zinc Finger-Containing Cellular Transcription Corepressor ZBTB25 Promotes Influenza Virus RNA Transcription and Is a Target for Zinc Ejector Drugs.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Influenza A virus (IAV) replication relies on an intricate interaction between virus and host cells. How the cellular proteins are usurped for IAV replication remains largely obscure. The aim of this study was to search for novel and potential cellular factors that participate in IAV replication. ZBTB25, a transcription repressor of a variety of cellular genes, was identified by an RNA interference (RNAi) genomic library screen. Depletion of ZBTB25 significantly reduced IAV production. Conversely, overexpression of ZBTB25 enhanced it. ZBTB25 interacted with the viral RNA-dependent RNA polymerase (RdRp) protein and modulated its transcription activity. In addition, ZBTB25 also functioned as a viral RNA (vRNA)-binding protein, binding preferentially to the U-rich sequence within the 5' untranslated region (UTR) of vRNA. Both protein-protein and protein-RNA interactions involving ZBTB25 facilitated viral RNA transcription and replication. In addition, ZBTB25 suppressed interferon production, further enhancing viral replication. ZBTB25-associated functions required an intact zinc finger domain and posttranslational SUMO-1 modification of ZBTB25. Furthermore, treatment with disulfiram (a zinc ejector) of ZBTB25-overexpressing cells showed significantly reduced IAV production as a result of reduced RNA synthesis. Our findings indicate that IAV usurps ZBTB25 for IAV RNA synthesis and serves as a novel and potential therapeutic antiviral target. IAV-induced seasonal influenza causes severe illness and death in high-risk populations. However, IAV has developed resistance to current antiviral drugs due to its high mutation rate. Therefore, development of drugs targeting cellular factors required for IAV replication is an attractive alternative for IAV therapy. Here, we discovered a cellular protein, ZBTB25, that enhances viral RdRp activity by binding to both viral RdRp and viral RNA to stimulate viral RNA synthesis. A unique feature of ZBTB25 in the regulation of viral replication is its dual transcription functions, namely, promoting viral RNA transcription through binding to the U-rich region of vRNA and suppressing cellular interferon production. ZBTB25 contains a zinc finger domain that is required for RNA-inhibitory activity by chelating zinc ions. Disulfiram treatment disrupts the zinc finger functions, effectively repressing IAV replication. Based on our findings, we demonstrate that ZBTB25 regulates IAV RNA transcription and replication and serves as a promising antiviral target for IAV treatment.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/metabolismo
Interações Hospedeiro-Patógeno
Vírus da Influenza A/genética
Proteínas Nucleares/metabolismo
Transcrição Genética
Zinco/metabolismo
[Mh] Termos MeSH secundário: Células A549
Antivirais/farmacologia
Proteínas de Ligação a DNA/deficiência
Proteínas de Ligação a DNA/genética
Dissulfiram/farmacologia
Células HEK293
Seres Humanos
Vírus da Influenza A/efeitos dos fármacos
Vírus da Influenza A/enzimologia
Vírus da Influenza A/fisiologia
Proteínas Nucleares/deficiência
Proteínas Nucleares/genética
Ligação Proteica
RNA Replicase/metabolismo
RNA Viral/metabolismo
Proteína SUMO-1/metabolismo
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (DNA-Binding Proteins); 0 (Nuclear Proteins); 0 (RNA, Viral); 0 (SUMO-1 Protein); 137951-89-4 (ZBTB25 protein, human); EC 2.7.7.48 (RNA Replicase); J41CSQ7QDS (Zinc); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


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[PMID]:28668395
[Au] Autor:Liu L; Huang C; Bian Y; Miao L
[Ad] Endereço:Clinical Pharmacology Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. Electronic address: linsheng_liu@126.com.
[Ti] Título:GC-MS based metabolomics of CSF and blood serum: Metabolic phenotype for a rat model of cefoperazone-induced disulfiram-like reaction.
[So] Source:Biochem Biophys Res Commun;490(3):1066-1073, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cefoperazone is most popularly used in the treatment of complicated infections clinically. Concomitant ingestion of ethnaol and cefoperazone may cause a disulfiram-like reaction. However, very little is known about the possible interactions between cefoperazone treatment and an alcohol with regard to the induction of disulfiram-like reaction. Study of the metabolic impact of cotreatment with cefoperazone and alcohol on animals can facilitate the identification of markers relevant to disulfiram-like reaction. In this study, the serum and cerebrospinal fluid (CSF) metabolites from Sprague-Dawley rats were profiled using gas chromatography mass spectrometry. Serum levels of valine, leucine, glycine, palmitelaidic acid, and 2-hydroxyisobutyrate in combination application group were significantly higher than those in the control; while alanine and pyruvate deceased in cotreatment group. Most TCA intermediates, glutamate and aspartate had lower CSF level in combination application group, except citrate. In addition, most carbohydrates, ethylmalonate and N-acetylaspartate had higher level compared with control group. These results highlight concomitant ingestion of alcohol and cefoperazone generated disulfiram-like reaction by way of disrupting normal metabolic pathway. Cefoperazone magnifes ethanol-induced impairment of TCA cycle and aspartate metabolism, thereby affects energy metabolism and neural transmission.
[Mh] Termos MeSH primário: Dissuasores de Álcool/farmacologia
Consumo de Bebidas Alcoólicas/sangue
Consumo de Bebidas Alcoólicas/líquido cefalorraquidiano
Antibacterianos/farmacologia
Cefoperazona/farmacologia
Dissulfiram/farmacologia
Metaboloma/efeitos dos fármacos
[Mh] Termos MeSH secundário: Consumo de Bebidas Alcoólicas/metabolismo
Animais
Etanol/farmacologia
Cromatografia Gasosa-Espectrometria de Massas/métodos
Masculino
Redes e Vias Metabólicas/efeitos dos fármacos
Metabolômica/métodos
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alcohol Deterrents); 0 (Anti-Bacterial Agents); 3K9958V90M (Ethanol); 7U75I1278D (Cefoperazone); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE


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[PMID]:28538998
[Au] Autor:Lyon J
[Ti] Título:More Treatments on Deck for Alcohol Use Disorder.
[So] Source:JAMA;317(22):2267-2269, 2017 Jun 13.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Dissuasores de Álcool/uso terapêutico
Transtornos Relacionados ao Uso de Álcool/tratamento farmacológico
[Mh] Termos MeSH secundário: Transtornos Relacionados ao Uso de Álcool/epidemiologia
Aminas/uso terapêutico
Baclofeno/uso terapêutico
Ácidos Cicloexanocarboxílicos/uso terapêutico
Citidina Difosfato Colina/uso terapêutico
Dissulfiram/uso terapêutico
Reposicionamento de Medicamentos
Frutose/análogos & derivados
Frutose/uso terapêutico
Seres Humanos
Mifepristona/uso terapêutico
Naltrexona/análogos & derivados
Naltrexona/uso terapêutico
National Institute on Alcohol Abuse and Alcoholism (U.S.)
Uso Off-Label
Aceitação pelo Paciente de Cuidados de Saúde/estatística & dados numéricos
Taurina/análogos & derivados
Taurina/uso terapêutico
Estados Unidos
Vareniclina/uso terapêutico
Ácido gama-Aminobutírico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alcohol Deterrents); 0 (Amines); 0 (Cyclohexanecarboxylic Acids); 0H73WJJ391 (topiramate); 1EQV5MLY3D (Taurine); 30237-26-4 (Fructose); 320T6RNW1F (Mifepristone); 536BQ2JVC7 (Cytidine Diphosphate Choline); 56-12-2 (gamma-Aminobutyric Acid); 5S6W795CQM (Naltrexone); 6CW7F3G59X (gabapentin); H789N3FKE8 (Baclofen); N4K14YGM3J (acamprosate); TOV02TDP9I (nalmefene); TR3MLJ1UAI (Disulfiram); W6HS99O8ZO (Varenicline)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170706
[Lr] Data última revisão:
170706
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.4760


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[PMID]:28344087
[Au] Autor:Djuric A; Begic A; Gobeljic B; Pantelic A; Zebic G; Stevanovic I; Djurdjevic D; Ninkovic M; Prokic V; Stanojevic I; Vojvodic D; Djukic M
[Ad] Endereço:Department for Toxicology, Faculty of Pharmacy, University of Belgrade, Vojvode Stepe 450, 11221 Belgrade, Serbia.
[Ti] Título:Subacute alcohol and/or disulfiram intake affects bioelements and redox status in rat testes.
[So] Source:Food Chem Toxicol;105:44-51, 2017 Jul.
[Is] ISSN:1873-6351
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of the study was to investigate if alcohol and disulfiram (DSF) individually and in combination affect bioelements' and red-ox homeostasis in testes of the exposed rats. The animals were divided into groups according to the duration of treatments (21 and/or 42 days): C /C groups (controls); OL and OL groups (0.5 mL olive oil intake); A groups (3 mL 20% ethanol intake); DSF groups (178.5 mg DSF/kg/day intake); and A +DSF groups (the DSF ingestion followed previous 21 days' treatment with alcohol). The measured parameters in testes included metals: zinc (Zn), copper (Cu), iron (Fe), magnesium (Mg) and selenium (Se); as well as oxidative stress (OS) parameters: superoxide anion radical (O ), glutathione reduced (GSH) and oxidized (GSSG), malondialdehyde (MDA), hydrogen peroxide (H O ) decomposition and activities of total superoxide dismutase (tSOD), glutathione-S-transferase (GST) and glutathione reductase (GR). Metal status was changed in all experimental groups (Fe rose, Zn fell, while Cu increased in A +DSF groups). Development of OS was demonstrated in A groups, but not in DSF groups. In A +DSF groups, OS was partially reduced compared to A groups (A >MDA>C; A
[Mh] Termos MeSH primário: Dissulfiram/metabolismo
Etanol/efeitos adversos
Estresse Oxidativo
Testículo/metabolismo
[Mh] Termos MeSH secundário: Animais
Dissulfiram/efeitos adversos
Etanol/metabolismo
Glutationa/metabolismo
Glutationa Transferase/metabolismo
Masculino
Malondialdeído/metabolismo
Oxirredução
Ratos
Ratos Wistar
Selênio/metabolismo
Superóxido Dismutase/metabolismo
Superóxidos/metabolismo
Testículo/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
11062-77-4 (Superoxides); 3K9958V90M (Ethanol); 4Y8F71G49Q (Malondialdehyde); EC 1.15.1.1 (Superoxide Dismutase); EC 2.5.1.18 (Glutathione Transferase); GAN16C9B8O (Glutathione); H6241UJ22B (Selenium); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE


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[PMID]:28220511
[Au] Autor:Goh ET; Morgan MY
[Ad] Endereço:UCL Institute for Liver & Digestive Health, Division of Medicine, Royal Free Campus, University College London, London, UK.
[Ti] Título:Review article: pharmacotherapy for alcohol dependence - the why, the what and the wherefore.
[So] Source:Aliment Pharmacol Ther;45(7):865-882, 2017 Apr.
[Is] ISSN:1365-2036
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The development of alcohol dependence is associated with significant morbidity and mortality. For the majority of affected people the most appropriate goal, in terms of drinking behaviour, is abstinence from alcohol. Psychosocial intervention is the mainstay of the treatment but adjuvant pharmacotherapy is also available and its use recommended. AIM: To provide an updated analysis of current and potential pharmacotherapeutic options for the management of alcohol dependence. In addition, factors predictive of therapeutic outcome, including compliance and pharmacogenetics, and the current barriers to treatment, including doctors' unwillingness to prescribe these agents, will be explored. METHODS: Relevant papers were selected for review following extensive, language- and date-unrestricted, electronic and manual searches of the literature. RESULTS: Acamprosate and naltrexone have a substantial evidence base for overall efficacy, safety and cost-effectiveness while the risks associated with the use of disulfiram are well-known and can be minimised with appropriate patient selection and supervision. Acamprosate can be used safely in patients with liver disease and in those with comorbid mental health issues and co-occurring drug-related problems. A number of other agents are being investigated for potential use for this indication including: baclofen, topiramate and metadoxine. CONCLUSION: Pharmacotherapy for alcohol dependence has been shown to be moderately efficacious with few safety concerns, but it is substantially underutilised. Concerted efforts must be made to remove the barriers to treatment in order to optimise the management of people with this condition.
[Mh] Termos MeSH primário: Dissuasores de Álcool/uso terapêutico
Alcoolismo/tratamento farmacológico
[Mh] Termos MeSH secundário: Alcoolismo/diagnóstico
Alcoolismo/genética
Baclofeno/uso terapêutico
Dissulfiram/uso terapêutico
Combinação de Medicamentos
Frutose/análogos & derivados
Frutose/uso terapêutico
Seres Humanos
Naltrexona/análogos & derivados
Naltrexona/uso terapêutico
Polimorfismo de Nucleotídeo Único
Piridoxina/uso terapêutico
Ácido Pirrolidonocarboxílico/uso terapêutico
Taurina/análogos & derivados
Taurina/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alcohol Deterrents); 0 (Drug Combinations); 0H73WJJ391 (topiramate); 1EQV5MLY3D (Taurine); 30237-26-4 (Fructose); 5S6W795CQM (Naltrexone); EJQ7M98H5J (metadoxine); H789N3FKE8 (Baclofen); KV2JZ1BI6Z (Pyridoxine); N4K14YGM3J (acamprosate); SZB83O1W42 (Pyrrolidonecarboxylic Acid); TOV02TDP9I (nalmefene); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.1111/apt.13965


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[PMID]:28182125
[Au] Autor:Wang C; Yang J; Han H; Chen J; Wang Y; Li Q; Wang Y
[Ad] Endereço:Department of Urology, First Hospital of Jilin University; Innovative Drug Research Centre, School of Pharmacy, Chongqing University, Chongqing.
[Ti] Título:Disulfiram-loaded porous PLGA microparticle for inhibiting the proliferation and migration of non-small-cell lung cancer.
[So] Source:Int J Nanomedicine;12:827-837, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:In this study, poly(lactic- -glycolic acid) (PLGA) was used as a carrier to construct disulfiram-loaded porous microparticle through the emulsion solvent evaporation method, using ammonium bicarbonate as a porogen. The microparticle possessed highly porous surface, suitable aerodynamic diameter for inhalation (8.31±1.33 µm), favorable drug loading (4.09%±0.11%), and sustained release profile. The antiproliferation effect of release supernatant was detected through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay using non-small-cell lung cancer A549 as a model, with only 13.3% of cell viability observed for the release supernatant at 7 days. The antiproliferation mechanism was elucidated to be associated with the enhanced induction of cell apoptosis and cell cycle arrest at S phase through flow cytometry and Western blotting analysis. Finally, wound healing and transwell migration assay showed that they could efficiently inhibit the cell migration. These results demonstrated that disulfiram-loaded porous PLGA microparticle could achieve favorable antitumor efficiency, implying the potential of treating non-small-cell lung cancer in a pulmonary administration.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/patologia
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Dissulfiram/farmacologia
Ácido Láctico/química
Neoplasias Pulmonares/patologia
Nanopartículas/química
Ácido Poliglicólico/química
[Mh] Termos MeSH secundário: Administração por Inalação
Dissuasores de Álcool/administração & dosagem
Dissuasores de Álcool/química
Dissuasores de Álcool/farmacologia
Western Blotting
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Dissulfiram/administração & dosagem
Dissulfiram/química
Seres Humanos
Neoplasias Pulmonares/tratamento farmacológico
Nanopartículas/administração & dosagem
Tamanho da Partícula
Porosidade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alcohol Deterrents); 0 (polylactic acid-polyglycolic acid copolymer); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); TR3MLJ1UAI (Disulfiram)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S121948



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