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[PMID]:27222379
[Au] Autor:Kheradmand A; Nayebi AM; Jorjani M; Khalifeh S; Haddadi R
[Ad] Endereço:Drug Applied Research Center, Department of Pharmacology and Toxicology, Tabriz University of Medical Sciences, Tabriz, Iran.
[Ti] Título:Effects of WR1065 on 6-hydroxydopamine-induced motor imbalance: Possible involvement of oxidative stress and inflammatory cytokines.
[So] Source:Neurosci Lett;627:7-12, 2016 Aug 03.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Over production of reactive oxygen species (ROS) is postulated to be the main contributor in degeneration of nigrostriatal dopaminergic neurons. In this study we investigated the effects of WR1065, a free radical scavenger, on motor imbalance, oxidative stress parameters and inflammatory cytokines in CSF and brain of hemi-parkinsonian rats. Lesion of dopaminergic neurons was done by unilateral infusion of 6-hydroxydopamine into the central region of the substentia nigra pars compacta (SNc) to induce hemi-parkinsonism and motor imbalance in rats. WR1065 (20, 40 and 80µg/2µl/rat) was administered three days before 6-OHDA administration. After three weeks behavioral study was performed and then brain and CSF samples were collected to assess tumor necrosis factor (TNFα), interlukin (IL-1ß), reduced glutathione (GSH), and malondialdehyde (MDA). WR1065 pre-treatment in rats before receiving 6-OHDA, improved significantly motor impairment and caused reduction of MDA and inflammatory cytokines TNFα and IL-1ß levels, while GSH level significantly increased when compared with lesioned rats. Our study indicated that WR1065 could improve 6-OHDA-induced motor imbalance. Furthermore, it decreased lipid peroxidation and inflammatory cytokines and restored the level of GSH up to normal range. We suggest that WR1065 can be proposed as a potential neuroprotective agent in motor impairments of PD. However to prove this hypothesis more clinical trial studies should be done.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Mercaptoetilaminas/administração & dosagem
Fármacos Neuroprotetores/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
Transtornos Parkinsonianos/prevenção & controle
Transtornos Parkinsonianos/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Glutationa/líquido cefalorraquidiano
Interleucina-1beta/líquido cefalorraquidiano
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Malondialdeído/líquido cefalorraquidiano
Atividade Motora/efeitos dos fármacos
Oxidopamina
Transtornos Parkinsonianos/líquido cefalorraquidiano
Transtornos Parkinsonianos/induzido quimicamente
Parte Compacta da Substância Negra/efeitos dos fármacos
Ratos
Ratos Wistar
Fator de Necrose Tumoral alfa/líquido cefalorraquidiano
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Mercaptoethylamines); 0 (Neuroprotective Agents); 0 (Tumor Necrosis Factor-alpha); 31098-42-7 (WR 1065); 4Y8F71G49Q (Malondialdehyde); 8HW4YBZ748 (Oxidopamine); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160526
[St] Status:MEDLINE


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[PMID]:26978566
[Au] Autor:Hofer M; Falk M; Komurková D; Falková I; Bacíková A; Klejdus B; Pagácová E; Stefancíková L; Weiterová L; Angelis KJ; Kozubek S; Dusek L; Galbavý S
[Ad] Endereço:Department of Cell Biology and Radiobiology, Institute of Biophysics, v.v.i., Czech Academy of Sciences , Královopolská 135, CZ-612 65 Brno, Czech Republic.
[Ti] Título:Two New Faces of Amifostine: Protector from DNA Damage in Normal Cells and Inhibitor of DNA Repair in Cancer Cells.
[So] Source:J Med Chem;59(7):3003-17, 2016 Apr 14.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Amifostine protects normal cells from DNA damage induction by ionizing radiation or chemotherapeutics, whereas cancer cells typically remain uninfluenced. While confirming this phenomenon, we have revealed by comet assay and currently the most sensitive method of DNA double strand break (DSB) quantification (based on γH2AX/53BP1 high-resolution immunofluorescence microscopy) that amifostine treatment supports DSB repair in γ-irradiated normal NHDF fibroblasts but alters it in MCF7 carcinoma cells. These effects follow from the significantly lower activity of alkaline phosphatase measured in MCF7 cells and their supernatants as compared with NHDF fibroblasts. Liquid chromatography-mass spectrometry confirmed that the amifostine conversion to WR-1065 was significantly more intensive in normal NHDF cells than in tumor MCF cells. In conclusion, due to common differences between normal and cancer cells in their abilities to convert amifostine to its active metabolite WR-1065, amifostine may not only protect in multiple ways normal cells from radiation-induced DNA damage but also make cancer cells suffer from DSB repair alteration.
[Mh] Termos MeSH primário: Amifostina/farmacologia
Dano ao DNA/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Protetores contra Radiação/farmacologia
[Mh] Termos MeSH secundário: Fosfatase Alcalina/genética
Fosfatase Alcalina/metabolismo
Amifostina/farmacocinética
Ensaio Cometa
Quebras de DNA de Cadeia Dupla/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Fibroblastos/efeitos da radiação
Raios gama
Histonas/genética
Histonas/metabolismo
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Células MCF-7/efeitos dos fármacos
Células MCF-7/efeitos da radiação
Mercaptoetilaminas/farmacocinética
Microscopia de Fluorescência/métodos
Proteína 1 de Ligação à Proteína Supressora de Tumor p53
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (H2AFX protein, human); 0 (Histones); 0 (Intracellular Signaling Peptides and Proteins); 0 (Mercaptoethylamines); 0 (Radiation-Protective Agents); 0 (TP53BP1 protein, human); 0 (Tumor Suppressor p53-Binding Protein 1); 31098-42-7 (WR 1065); EC 3.1.3.1 (Alkaline Phosphatase); M487QF2F4V (Amifostine)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160316
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.5b01628


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[PMID]:26452927
[Au] Autor:Na W; Liu S; Liu X; Su X
[Ad] Endereço:Department of Analytical Chemistry, College of Chemistry, Jilin University, Changchun 130012, China.
[Ti] Título:Ultrasensitive detection of amifostine and alkaline phosphatase based on the growth of CdS quantum dots.
[So] Source:Talanta;144:1059-64, 2015 Nov 01.
[Is] ISSN:1873-3573
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In this study, we reported a simple and sensitive fluorescence nanosensor for rapid detection of amifostine and alkaline phosphatase (ALP). The novel nanosensor was based on the fluorescence "turn on-off" of CdS quantum dots (QDs). Firstly, Cd(2+) cation could react with S(2-) anion to generate fluorescent CdS QDs in the presence of amifostine. The fluorescence (FL) intensity of amifostine-capped CdS QDs (Amifostine-CdS QDs) was increased with the increasing amounts of amifostine, and could be used for amifostine detection. However, amifostine could be converted to 2-(3-aminopropylamino) ethanethiol (WR1065) in the presence of ALP based on the dephosphorylation of ALP. Under the optimum conditions, the affinity of WR1065 to CdS QDs was weaker than that of amifostine. Therefore the new generation of WR1065-CdS QDs would reduce the FL intensity with the increase of ALP concentration, and the fluorescence of CdS QDs was turn off. The metabolic process of amifostine in the presence of alkaline phosphatase could be also studied via the change of FL intensity of CdS QDs. The present method was cost-effective, convenient, and does not require any complicated synthetic procedures.
[Mh] Termos MeSH primário: Fosfatase Alcalina/análise
Amifostina/análise
Compostos de Cádmio/química
Limite de Detecção
Nanotecnologia/instrumentação
Pontos Quânticos/química
Sulfetos/química
[Mh] Termos MeSH secundário: Fosfatase Alcalina/sangue
Fosfatase Alcalina/metabolismo
Amifostina/química
Seres Humanos
Hidrólise
Mercaptoetilaminas/química
Ácidos Fosfóricos/química
Fosforilação
Espectrometria de Fluorescência
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cadmium Compounds); 0 (Mercaptoethylamines); 0 (Phosphoric Acids); 0 (Sulfides); 057EZR4Z7Q (cadmium sulfide); 31098-42-7 (WR 1065); E4GA8884NN (phosphoric acid); EC 3.1.3.1 (Alkaline Phosphatase); M487QF2F4V (Amifostine)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:151010
[Lr] Data última revisão:
151010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151011
[St] Status:MEDLINE


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[PMID]:26222219
[Au] Autor:Chen CH; Kuo ML; Wang JL; Liao WC; Chang LC; Chan LP; Lin J
[Ad] Endereço:*Institute of Toxicology, College of Medicine, †Institute of Biochemical Sciences, College of Life Science, National Taiwan University, Taipei, Taiwan; ‡Institute of Basic Medical Sciences, National Cheng Kung University, College of Medicine, Tainan, Taiwan; §Department of Occupational Therapy, I-Shou University, Kaohsiung, Taiwan; §§Institute of Clinical Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; **Department of Otolaryngology-Head and Neck Surgery, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan; ††Department of Hematology, Mackay Memorial Hospital, Taipei, Taiwan.
[Ti] Título:CCM-AMI, a Polyethylene Glycol Micelle with Amifostine, as an Acute Radiation Syndrome Protectant in C57BL/6 Mice.
[So] Source:Health Phys;109(3):242-8, 2015 Sep.
[Is] ISSN:1538-5159
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute radiation syndrome results from radiation exposure, such as in accidental nuclear disasters. Safe and effective radioprotectants, mitigators, and treatment drugs must be developed as medical countermeasures against radiation exposure. Here, the authors evaluated CCM-Ami, a novel polyethylene glycol micelle encapsulated with amifostine, for its radioprotective properties after total-body irradiation from a 60Co source. Male C57BL/6 mice (6-8 wk old) were intravenously injected with 45 mg kg(-1) of CCM-Ami 90 min before exposure to 7.2 and 8.5 Gy irradiation at a dose rate of 0.04 Gy min(-1). Both survival benefit and hematopoietic protection were observed after prophylactic CCM-Ami administration when compared with the effects measured in excipient control and amifostine groups. Pharmacokinetic results showed that after the intravenous injection, the plasma concentration of WR-1065, the active form of amifostine, was higher in CCM-Ami-treated mice than in amifostine-treated mice. These findings suggest that CCM-Ami-mediated hematopoietic protection plays a key role in enhancing survival of mice exposed to radiation toxicity and thus indicate that CCM-Ami is a radioprotectant that can be used safely and effectively in nuclear disasters.
[Mh] Termos MeSH primário: Síndrome Aguda da Radiação/prevenção & controle
Amifostina/administração & dosagem
Protetores contra Radiação/administração & dosagem
[Mh] Termos MeSH secundário: Síndrome Aguda da Radiação/sangue
Amifostina/farmacocinética
Animais
Modelos Animais de Doenças
Relação Dose-Resposta à Radiação
Masculino
Mercaptoetilaminas/sangue
Camundongos
Camundongos Endogâmicos C57BL
Micelas
Polietilenoglicóis
Protetores contra Radiação/farmacocinética
Irradiação Corporal Total
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mercaptoethylamines); 0 (Micelles); 0 (Radiation-Protective Agents); 30IQX730WE (Polyethylene Glycols); 31098-42-7 (WR 1065); M487QF2F4V (Amifostine)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150730
[St] Status:MEDLINE
[do] DOI:10.1097/HP.0000000000000326


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[PMID]:26188467
[Au] Autor:Crowe ME; Lieven CJ; Thompson AF; Sheibani N; Levin LA
[Ad] Endereço:Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States.
[Ti] Título:Borane-protected phosphines are redox-active radioprotective agents for endothelial cells.
[So] Source:Redox Biol;6:73-9, 2015 Dec.
[Is] ISSN:2213-2317
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Exposure to radiation can damage endothelial cells in the irradiated area via the production of reactive oxygen species. We synthesized phosphine-borane complexes that reduce disulfide bonds and had previously been shown to interfere with redox-mediated signaling of cell death. We hypothesized that this class of drugs could interfere with the downstream effects of oxidative stress after irradiation and rescue endothelial cells from radiation damage. Cultured bovine aortic endothelial cells were plated for clonogenic assay prior to exposure to varying doses of irradiation from a (137)Cs irradiator and treated with various concentrations of bis(3-propionic acid methyl ester)phenylphosphine borane complex (PB1) at different time points. The clone-forming ability of the irradiated cells was assessed seven days after irradiation. We compared the radioprotective effects of PB1 with the aminothiol radioprotectant WR1065 and known superoxide scavengers. PB1 significantly protected bovine aortic endothelial cells from radiation damage, particularly when treated both before and after radiation. The radioprotection with 1 µM PB1 corresponded to a dose-reduction factor of 1.24. Radioprotection by PB1 was comparable to the aminothiol WR1065, but was significantly less toxic and required much lower concentrations of drug (1 µM vs. 4 mM, respectively). Superoxide scavengers were not radioprotective in this paradigm, indicating the mechanisms for both loss of clonogenicity and PB1 radioprotection are independent of superoxide signaling. These data demonstrate that PB1 is an effective redox-active radioprotectant for endothelial cells in vitro, and is radioprotective at a concentration approximately 4 orders of magnitude lower than the aminothiol WR1065 with less toxicity.
[Mh] Termos MeSH primário: Boranos/farmacologia
Células Endoteliais/efeitos dos fármacos
Raios gama/efeitos adversos
Fosfinas/farmacologia
Protetores contra Radiação/farmacologia
Superóxidos/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Aorta/citologia
Aorta/efeitos dos fármacos
Aorta/metabolismo
Aorta/efeitos da radiação
Bovinos
Células Cultivadas
Células Clonais
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Células Endoteliais/efeitos da radiação
Seres Humanos
Mercaptoetilaminas/farmacologia
Metaloporfirinas/farmacologia
Oxirredução
Polietilenoglicóis/farmacologia
Transdução de Sinais
Superóxido Dismutase/farmacologia
Superóxidos/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 (Boranes); 0 (Mercaptoethylamines); 0 (Metalloporphyrins); 0 (Mn(III) 5,10,15,20-tetrakis(N-methylpyridinium-2-yl)porphyrin); 0 (Phosphines); 0 (Radiation-Protective Agents); 0 (bis(3-propionic acid methyl ester)phenylphosphine borane complex); 11062-77-4 (Superoxides); 30IQX730WE (Polyethylene Glycols); 31098-42-7 (WR 1065); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (polyethylene glycol-superoxide dismutase)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150720
[St] Status:MEDLINE


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[PMID]:25407396
[Au] Autor:Omar SI; Tuszynski J
[Ad] Endereço:Department of Oncology, University of Alberta, Edmonton, AB, Canada, T6G 1Z2.
[Ti] Título:Ranking the Binding Energies of p53 Mutant Activators and Their ADMET Properties.
[So] Source:Chem Biol Drug Des;86(2):163-72, 2015 Aug.
[Is] ISSN:1747-0285
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The guardian of the genome, p53, is the most mutated protein found in all cancer cells. Restoration of wild-type activity to mutant p53 offers promise to eradicate cancer cells using novel pharmacological agents. Several molecules have already been found to activate mutant p53. While the exact mechanism of action of these compounds has not been fully understood, a transiently open pocket has been identified in some mutants. In our study, we docked twelve known activators to p53 into the open pocket to further understand their mechanism of action and rank the best binders. In addition, we predicted the absorption, distribution, metabolism, excretion and toxicity properties of these compounds to assess their pharmaceutical usefulness. Our studies showed that alkylating ligands do not all bind at the same position, probably due to their varying sizes. In addition, we found that non-alkylating ligands are capable of binding at the same pocket and directly interacting with Cys124. The comparison of the different ligands demonstrates that stictic acid has a great potential as a p53 activator in terms of less adverse effects although it has poorer pharmacokinetic properties.
[Mh] Termos MeSH primário: Proteína Supressora de Tumor p53/química
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Alquilação
Amifostina/química
Amifostina/farmacocinética
Amifostina/toxicidade
Compostos Aza/química
Compostos Aza/farmacocinética
Compostos Aza/toxicidade
Compostos Bicíclicos Heterocíclicos com Pontes/química
Compostos Bicíclicos Heterocíclicos com Pontes/farmacocinética
Compostos Bicíclicos Heterocíclicos com Pontes/toxicidade
Avaliação Pré-Clínica de Medicamentos
Elipticinas/química
Elipticinas/farmacocinética
Elipticinas/farmacologia
Elipticinas/toxicidade
Compostos Heterocíclicos de 4 ou mais Anéis/química
Compostos Heterocíclicos de 4 ou mais Anéis/farmacocinética
Compostos Heterocíclicos de 4 ou mais Anéis/toxicidade
Seres Humanos
Cinética
Ligantes
Mercaptoetilaminas/química
Mercaptoetilaminas/farmacocinética
Mercaptoetilaminas/toxicidade
Simulação de Dinâmica Molecular
Mutagênese Sítio-Dirigida
Mutação
Oxepinas/química
Oxepinas/farmacocinética
Oxepinas/toxicidade
Ligação Proteica
Pirimidinas/química
Pirimidinas/farmacologia
Pirimidinas/toxicidade
Quinuclidinas/química
Quinuclidinas/farmacocinética
Quinuclidinas/toxicidade
Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-one); 0 (2-hydroxymethyl-2-methoxymethylazabicyclo(2.2.2)octan-3-one); 0 (Aza Compounds); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (Ellipticines); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (Ligands); 0 (Mercaptoethylamines); 0 (Oxepins); 0 (Pyrimidines); 0 (Quinuclidines); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 0 (stictic acid); 117VLW7484 (ellipticine); 31098-42-7 (WR 1065); 9G4A3ET6XG (9-hydroxyellipticine); IN3WH41H3A (CP 31398); M487QF2F4V (Amifostine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141120
[St] Status:MEDLINE
[do] DOI:10.1111/cbdd.12480


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[PMID]:24833597
[Au] Autor:Olivero OA; Ongele MO; Braun HM; Marrogi A; Divi K; Mitchell JB; Poirier MC
[Ad] Endereço:Carcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
[Ti] Título:Selective protection of zidovudine-induced DNA-damage by the antioxidants WR-1065 and tempol.
[So] Source:Environ Mol Mutagen;55(7):566-72, 2014 Aug.
[Is] ISSN:1098-2280
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cytokinesis-block micronucleus cytome (CBMN) assay, introduced by Fenech, was used to demonstrate different types of DNA damage in MOLT-3 human lymphoblastoid cells exposed to 10 µM zidovudine (AZT). In addition, we explored the cytoprotective potential of two antioxidants, WR-1065 and Tempol, to decrease AZT-induced genotoxicity. Binucleated cells, arrested by Cytochalasin B (Cyt B), were evaluated for micronuclei (MN), caused by DNA damage or chromosomal loss, and chromatin nucleoplasmic bridges (NPBs), caused by telomere attrition. Additionally, nuclear buds (NBUDs), caused by amplified DNA, and apoptotic and necrotic (A/N) cells were scored. We hypothesized that AZT exposure would increase the frequency of genotoxic end points, and that the antioxidants Tempol and WR-1065 would protect against AZT-induced genotoxicity. MOLT-3 cells were exposed to 0 or 10 µM AZT for a total of 76 hr. After the first 24 hr, 0 or 5 µM WR-1065 and/or 0 or 200 µM Tempol were added for the remainder of the experiment. For the last 28 hr (of 76 hr), Cyt B was added to arrest replication after one cell division, leaving a predominance of binucleated cells. The nuclear division index (NDI) was similar for all treatment groups, indicating that the exposures did not alter cell viability. MOLT-3 cells exposed to AZT alone had significant (P < 0.05) increases in MN and NBs, compared to unexposed cells. Both Tempol and WR-1065 protected against AZT-induced MN formation (P < 0.003 for both), and WR-1065, but not Tempol, reduced the levels of A/N (P = 0.041). In cells exposed to AZT/Tempol there were significantly reduced levels of NBUDs, compared to cells exposed to AZT alone (P = 0.015). Cells exposed to AZT/WR-1065 showed reduced levels of NPBs, compared to cells exposed to AZT alone (P = 0.037). Thus WR-1065 and Tempol protected MOLT-3 cells against specific types of AZT-induced DNA damage.
[Mh] Termos MeSH primário: Antioxidantes/química
Cromatina/química
Óxidos N-Cíclicos/química
Dano ao DNA
Mercaptoetilaminas/química
Zidovudina/química
[Mh] Termos MeSH secundário: Apoptose
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Proliferação Celular
Sobrevivência Celular
Cromossomos/ultraestrutura
Citocalasina B/química
Seres Humanos
Testes para Micronúcleos
Mutagênicos/química
Necrose
Protetores contra Radiação/química
Marcadores de Spin
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Antioxidants); 0 (Chromatin); 0 (Cyclic N-Oxides); 0 (Mercaptoethylamines); 0 (Mutagens); 0 (Radiation-Protective Agents); 0 (Spin Labels); 31098-42-7 (WR 1065); 3CHI920QS7 (Cytochalasin B); 4B9XT59T7S (Zidovudine); U78ZX2F65X (tempol)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140517
[St] Status:MEDLINE
[do] DOI:10.1002/em.21872


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[PMID]:24688895
[Au] Autor:Vidal N; Cavaille JP; Graziani F; Robin M; Ouari O; Pietri S; Stocker P
[Ad] Endereço:Aix Marseille Université, CNRS, ICR UMR 7273, 13397, Marseille, France.
[Ti] Título:High throughput assay for evaluation of reactive carbonyl scavenging capacity.
[So] Source:Redox Biol;2:590-8, 2014.
[Is] ISSN:2213-2317
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Many carbonyl species from either lipid peroxidation or glycoxidation are extremely reactive and can disrupt the function of proteins and enzymes. 4-hydroxynonenal and methylglyoxal are the most abundant and toxic lipid-derived reactive carbonyl species. The presence of these toxics leads to carbonyl stress and cause a significant amount of macromolecular damages in several diseases. Much evidence indicates trapping of reactive carbonyl intermediates may be a useful strategy for inhibiting or decreasing carbonyl stress-associated pathologies. There is no rapid and convenient analytical method available for the assessment of direct carbonyl scavenging capacity, and a very limited number of carbonyl scavengers have been identified to date, their therapeutic potential being highlighted only recently. In this context, we have developed a new and rapid sensitive fluorimetric method for the assessment of reactive carbonyl scavengers without involvement glycoxidation systems. Efficacy of various thiol- and non-thiol-carbonyl scavenger pharmacophores was tested both using this screening assay adapted to 96-well microplates and in cultured cells. The scavenging effects on the formation of Advanced Glycation End-product of Bovine Serum Albumin formed with methylglyoxal, 4-hydroxynonenal and glucose-glycated as molecular models were also examined. Low molecular mass thiols with an α-amino-ß-mercaptoethane structure showed the highest degree of inhibitory activity toward both α,ß-unsaturated aldehydes and dicarbonyls. Cysteine and cysteamine have the best scavenging ability toward methylglyoxal. WR-1065 which is currently approved for clinical use as a protective agent against radiation and renal toxicity was identified as the best inhibitor of 4-hydroxynonenal.
[Mh] Termos MeSH primário: Aldeídos/farmacologia
Cisteamina/farmacologia
Cisteína/farmacologia
Ensaios de Triagem em Larga Escala/métodos
Aldeído Pirúvico/farmacologia
[Mh] Termos MeSH secundário: Aldeídos/antagonistas & inibidores
Animais
Células CACO-2
Linhagem Celular Tumoral
Produtos Finais de Glicação Avançada/metabolismo
Seres Humanos
Mercaptoetilaminas/farmacologia
Camundongos
Aldeído Pirúvico/antagonistas & inibidores
Sensibilidade e Especificidade
Soroalbumina Bovina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aldehydes); 0 (Glycation End Products, Advanced); 0 (Mercaptoethylamines); 27432CM55Q (Serum Albumin, Bovine); 31098-42-7 (WR 1065); 5UX2SD1KE2 (Cysteamine); 722KLD7415 (Pyruvaldehyde); K1CVM13F96 (4-hydroxy-2-nonenal); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140402
[St] Status:MEDLINE
[do] DOI:10.1016/j.redox.2014.01.016


  9 / 514 MEDLINE  
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[PMID]:23736649
[Au] Autor:Li C; Wang S; Huang T; Chen N; Ou M
[Ad] Endereço:Department of Otorhinolaryngology, Eye-Ear-Nose-Throat Hospital of Fudan University, Shanghai, China.
[Ti] Título:Feasibility study of the pharmacology of local application of amifostine (WR-2721) to the buccal mucosa in guinea pigs.
[So] Source:Pharmacology;91(5-6):281-6, 2013.
[Is] ISSN:1423-0313
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: We have undertaken this study to investigate the feasibility of topical application of the radioprotective compound WR-2721 to the buccal mucosa. METHODS: Saliva samples were collected from 5 volunteers and were reconstituted in 3 amifostine solutions. Measurements of amifostine and WR-1065 contents were performed at 6 different time points. Young-adult guinea pigs were topically administered amifostine 50 and 100 mg to each buccal mucosa. At 0, 15 and 30 min after application, the blood samples obtained from the heart and the buccal tissues were prepared for the analysis of amifostine and WR-1065. RESULTS: There was no significant difference between the 3 concentrations of amifostine in saliva in vitro at any of the 6 study time points (p > 0.05). No WR-1065 was detected in saliva. In the guinea pigs from groups A and B, there were significant differences in concentrations of amifostine and WR-1065 in the tissues between the 0-min and 15-min subgroups and between the 0-min and 30-min subgroups (p < 0.05). The concentrations of amifostine and WR-1065 from the 15-min and 30-min subgroups did not differ statistically (p > 0.05). CONCLUSIONS: It is feasible to administer topical amifostine (WR-2721) to mucosa to prevent radiation-induced oral mucositis, and systemic absorption is negligible. Relatively high concentrations of amifostine in human saliva in vitro were maintained, although some inconsistent changes are observed.
[Mh] Termos MeSH primário: Amifostina/administração & dosagem
Amifostina/farmacocinética
Mucosa Bucal/metabolismo
Protetores contra Radiação/administração & dosagem
Protetores contra Radiação/farmacocinética
[Mh] Termos MeSH secundário: Administração Bucal
Animais
Estudos de Viabilidade
Cobaias
Seres Humanos
Mercaptoetilaminas/metabolismo
Miocárdio/metabolismo
Saliva/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mercaptoethylamines); 0 (Radiation-Protective Agents); 31098-42-7 (WR 1065); M487QF2F4V (Amifostine)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:130724
[Lr] Data última revisão:
130724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130606
[St] Status:MEDLINE
[do] DOI:10.1159/000350396


  10 / 514 MEDLINE  
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[PMID]:23643735
[Au] Autor:Samiei N; Mangas-Sanjuan V; González-Álvarez I; Foroutan M; Shafaati A; Zarghi A; Bermejo M
[Ad] Endereço:Department of Engineering, Pharmacy Section, Miguel Hernandez University, Carretera Alicante Valencia km 87, 03550 San Juan de Alicante, Alicante, Spain.
[Ti] Título:Ion-pair strategy for enabling amifostine oral absorption: rat in situ and in vivo experiments.
[So] Source:Eur J Pharm Sci;49(4):499-504, 2013 Jul 16.
[Is] ISSN:1879-0720
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study shows the effect of ion pair formation on intestinal absorption and oral bioavailability of amifostine. Amifostine is a prodrug used as a highly potent and selective radiotherapy and chemotherapy protectant but due to its low lipophilicity and charge at physiological pH range, its trans epithelial transport and its potential for oral drug delivery is very low. Ion pair formation with negatively charged counter ions was evaluated by in situ rat perfusion studies as a possible strategy to enhance intestinal absorption of amifostine. Succinic acid, phthalic acid and benzoic acid were used as counter ions. Rat intestinal perfusion studies confirmed a statistically significant increase in amifostine permeability in the presence of the counter ions in the order of succinic>phthalic>benzoic. Rat pharmacokinetic studies in vivo were performed to calculate oral absolute bioavailability of amifostine alone and with ion pairs in order to confirm the in situ perfusion results and the applicability of the ion pair approach. Intravenous and intraduodenal administrations were done in rats using a permanent jugular vein cannulation technique and a duodenal cannulation method to avoid drug degradation in stomach. In vivo oral bioavailability studies demonstrated a 20-30-fold increase in amifostine bioavailability with succinic acid depending on counter ion ratio and 10-fold increase with phthalic acid as ion pair. In summary ion pair strategy with succinic acid could enable amifostine oral administration on enteric coated formulations.
[Mh] Termos MeSH primário: Amifostina/administração & dosagem
Absorção Intestinal
Ácidos Ftálicos/administração & dosagem
Protetores contra Radiação/administração & dosagem
Ácido Succínico/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Amifostina/farmacocinética
Animais
Ácido Benzoico/administração & dosagem
Disponibilidade Biológica
Intestino Delgado/metabolismo
Masculino
Mercaptoetilaminas/sangue
Perfusão
Pró-Fármacos
Protetores contra Radiação/farmacocinética
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mercaptoethylamines); 0 (Phthalic Acids); 0 (Prodrugs); 0 (Radiation-Protective Agents); 31098-42-7 (WR 1065); 6O7F7IX66E (phthalic acid); 8SKN0B0MIM (Benzoic Acid); AB6MNQ6J6L (Succinic Acid); M487QF2F4V (Amifostine)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130507
[St] Status:MEDLINE



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