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Pesquisa : D02.691.850.900.910 [Categoria DeCS]
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[PMID]:19422909
[Au] Autor:Röhl C; Grell M; Maser E
[Ad] Endereço:Institute of Toxicology and Pharmacology for Natural Scientists, Christian-Albrechts-University of Kiel, Brunswiker Str. 10, D-24105 Kiel, Germany. claudia.roehl@gmx.net
[Ti] Título:The organotin compounds trimethyltin (TMT) and triethyltin (TET) but not tributyltin (TBT) induce activation of microglia co-cultivated with astrocytes.
[So] Source:Toxicol In Vitro;23(8):1541-7, 2009 Dec.
[Is] ISSN:1879-3177
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The organotin compounds trimethyltin (TMT), triethyltin (TET) and tributyltin (TBT) show different organotoxicities in vivo. While TMT and TET induce a strong neurotoxicity accompanied by microglial and astroglial activation, TBT rather effects the immune system. Previously, we have shown in an in vitro co-culture model that microglial cells can be activated by TMT in the presence of astrocytes. In this study, we wanted to investigate (a) if the neurotoxic organotin compound TET can also activate microglial cells in vitro similar to TMT and (b) if differences between the neurotoxicants TMT and TET on the one side and TBT on the other exist concerning microglial activation. Therefore, purified microglial and astroglial cell cultures from neonatal rat brains were treated either alone or in co-cultures for 24h with different concentrations of TMT, TET or TBT and the basal cytotoxicity and nitric oxide formation was determined. Furthermore, morphological changes of astrocytes were examined. Our results show that microglial activation can be increased in subcytolethal concentrations, but only in the presence of astrocytes and not in microglial cell cultures alone. This increase was induced by the neurotoxicants TMT and TET but not by TBT. Taken together, the differing microglia activating effect of the organotin compounds may contribute to the differing neurotoxic potential of this group of chemicals in vivo. In addition, our results emphasize the need for co-culture systems when studying interactions between different cell types for toxicity assessment.
[Mh] Termos MeSH primário: Astrócitos/efeitos dos fármacos
Microglia/efeitos dos fármacos
Compostos de Trialquitina/toxicidade
Compostos de Trietilestanho/toxicidade
Compostos de Trimetilestanho/toxicidade
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Técnicas de Cocultura
Relação Dose-Resposta a Droga
Óxido Nítrico/biossíntese
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Trialkyltin Compounds); 0 (Triethyltin Compounds); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin); 31C4KY9ESH (Nitric Oxide); 4XDX163P3D (tributyltin); 5XCT3EQJ85 (triethyltin)
[Em] Mês de entrada:1001
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090509
[St] Status:MEDLINE
[do] DOI:10.1016/j.tiv.2009.04.013


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Bruzzo, Cristina
Texto completo
[PMID]:18563295
[Au] Autor:Alama A; Viale M; Cilli M; Bruzzo C; Novelli F; Tasso B; Sparatore F
[Ad] Endereço:Tumor Genetic, Lung Cancer Unit, National Institute for Cancer Research, Largo R. Benzi 10, 16132, Genoa, Italy. angela.alama@istge.it
[Ti] Título:In vitro cytotoxic activity of tri-n-butyltin(IV)lupinylsulfide hydrogen fumarate (IST-FS 35) and preliminary antitumor activity in vivo.
[So] Source:Invest New Drugs;27(2):124-30, 2009 Apr.
[Is] ISSN:1573-0646
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cytotoxicity in vitro and antitumor activity in vivo of the organotin compound tri-n-butyltin(IV)lupinylsulfide hydrogen fumarate (IST-FS 35) have been investigated. The IC50 values obtained in a panel of tumor cell lines were compared to those of the parental compound IST-FS 29 in the same cells. IST-FS 35 resulted significantly more active than IST-FS 29 with IC50 values in the range 0.16-1.8 microM. Toxicity studies in vivo, after intravenous administration of escalating concentrations of IST-FS 35, provided the identification of the maximal tolerated dose (3.5 mg/kg) which was employed as therapeutic dose in the antitumor activity experiments. Preliminary results, in transplanted murine tumor models, revealed that both the P388 myelomonocytic leukaemia and the B16-F10 melanoma, implanted subcutaneously in BDF1 mice, were inhibited about 96% in their tumor volume at day 11, following a single intravenous injection of the compound. Additional studies are mandatory to unravel the mechanism of action for the development of IST-FS 35 as potential antitumor drug.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Compostos Orgânicos de Estanho/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Feminino
Seres Humanos
Concentração Inibidora 50
Leucemia P388
Dose Máxima Tolerável
Melanoma Experimental
Camundongos
Compostos Orgânicos de Estanho/efeitos adversos
Compostos Orgânicos de Estanho/química
Compostos de Trietilestanho/química
Compostos de Trietilestanho/uso terapêutico
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (IST-FS 29); 0 (IST-FS 35); 0 (Organotin Compounds); 0 (Triethyltin Compounds)
[Em] Mês de entrada:0906
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080620
[St] Status:MEDLINE
[do] DOI:10.1007/s10637-008-9148-x


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[PMID]:17632591
[Au] Autor:Girard P; Verniers D; Pansart Y; Gillardin JM
[Ad] Endereço:Biocodex, Service de Pharmacologie, Zac de Mercières 60200 Compiègne, France. p.girard@biocodex.fr
[Ti] Título:Efficacy of moclobemide in a rat model of neurotoxicant-induced edema.
[So] Source:Can J Physiol Pharmacol;85(5):556-61, 2007 May.
[Is] ISSN:0008-4212
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:The potent antidepressant effect of moclobemide, a selective and reversible type A monoamine oxidase (MAO) inhibitor, is clinically established. In view of the ongoing debate on the neuroprotective properties of MAO inhibitors, the present study was undertaken to further define the protective effect of moclobemide in a rat model of neurotoxicant-induced edema. In this model, daily oral triethyltin (TET) administration for 5 consecutive days strongly perturbed the rat behaviour and induced a cerebral edema at the 5th day. Oral coadministration of moclobemide (2 x 100 mg.kg-1.day-1) with TET blocked the development of brain edema and the increase in the cerebral chloride content induced by TET. Moreover, moclobemide reduced the increase in the cerebral sodium content and attenuated the neurological deficit. In conclusion, moclobemide possesses potent protective properties in this rat model of cerebral edema, suggesting potential clinical utility as a neuroprotectant.
[Mh] Termos MeSH primário: Edema Encefálico/prevenção & controle
Moclobemida/farmacologia
Compostos de Trietilestanho/toxicidade
[Mh] Termos MeSH secundário: Administração Oral
Animais
Índice de Massa Corporal
Edema Encefálico/induzido quimicamente
Edema Encefálico/fisiopatologia
Cálcio/metabolismo
Córtex Cerebral/química
Córtex Cerebral/efeitos dos fármacos
Córtex Cerebral/patologia
Cloretos/metabolismo
Relação Dose-Resposta a Droga
Intubação Gastrointestinal
Masculino
Moclobemida/administração & dosagem
Moclobemida/uso terapêutico
Monoaminoxidase/efeitos dos fármacos
Inibidores da Monoaminoxidase/administração & dosagem
Inibidores da Monoaminoxidase/farmacocinética
Inibidores da Monoaminoxidase/uso terapêutico
Atividade Motora/efeitos dos fármacos
Síndromes Neurotóxicas/etiologia
Síndromes Neurotóxicas/fisiopatologia
Síndromes Neurotóxicas/prevenção & controle
Potássio/metabolismo
Ratos
Ratos Wistar
Sódio/metabolismo
Fatores de Tempo
Resultado do Tratamento
Compostos de Trietilestanho/administração & dosagem
Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chlorides); 0 (Monoamine Oxidase Inhibitors); 0 (Triethyltin Compounds); 059QF0KO0R (Water); 9NEZ333N27 (Sodium); EC 1.4.3.4 (Monoamine Oxidase); PJ0Y7AZB63 (Moclobemide); RWP5GA015D (Potassium); SY7Q814VUP (Calcium); UOP17166KC (bromotriethylstannane)
[Em] Mês de entrada:0710
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070717
[St] Status:MEDLINE


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[PMID]:16135027
[Au] Autor:Yu ZF; Catalano PJ
[Ad] Endereço:Statistics Collaborative, Inc., 1710 Rhode Island Avenue, Suite 200, Washington, DC 20036, USA. fan-fan@statcollab.com
[Ti] Título:Quantitative risk assessment for multivariate continuous outcomes with application to neurotoxicology: the bivariate case.
[So] Source:Biometrics;61(3):757-66, 2005 Sep.
[Is] ISSN:0006-341X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The neurotoxic effects of chemical agents are often investigated in controlled studies on rodents, with multiple binary and continuous endpoints routinely collected. One goal is to conduct quantitative risk assessment to determine safe dose levels. Such studies face two major challenges for continuous outcomes. First, characterizing risk and defining a benchmark dose are difficult. Usually associated with an adverse binary event, risk is clearly definable in quantal settings as presence or absence of an event; finding a similar probability scale for continuous outcomes is less clear. Often, an adverse event is defined for continuous outcomes as any value below a specified cutoff level in a distribution assumed normal or log normal. Second, while continuous outcomes are traditionally analyzed separately for such studies, recent literature advocates also using multiple outcomes to assess risk. We propose a method for modeling and quantitative risk assessment for bivariate continuous outcomes that address both difficulties by extending existing percentile regression methods. The model is likelihood based; it allows separate dose-response models for each outcome while accounting for the bivariate correlation and overall characterization of risk. The approach to estimation of a benchmark dose is analogous to that for quantal data without the need to specify arbitrary cutoff values. We illustrate our methods with data from a neurotoxicity study of triethyl tin exposure in rats.
[Mh] Termos MeSH primário: Modelos Estatísticos
Doenças do Sistema Nervoso Periférico/induzido quimicamente
Medição de Risco/métodos
Testes de Toxicidade/métodos
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Seres Humanos
Funções Verossimilhança
Análise Multivariada
Sistema Nervoso Periférico/efeitos dos fármacos
Ratos
Compostos de Trietilestanho/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Triethyltin Compounds); 5XCT3EQJ85 (triethyltin)
[Em] Mês de entrada:0511
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050902
[St] Status:MEDLINE


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[PMID]:15869831
[Au] Autor:Zhu Y; Jia Z; Wang W; Gift JS; Moser VC; Pierre-Louis BJ
[Ad] Endereço:Department of Epidemiology and Biostatistics, University of South Florida, Tampa, FL 33612, USA. yzhu@hsc.usf.edu
[Ti] Título:Analyses of neurobehavioral screening data: benchmark dose estimation.
[So] Source:Regul Toxicol Pharmacol;42(2):190-201, 2005 Jul.
[Is] ISSN:0273-2300
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Zhu et al. (Zhu, Y., Wessel, M., Liu, T., Moser, V.C., 2005. Analyses of neurobehavioral screening data: dose-time-response modeling of continuous outcomes. Regul. Toxicol. Pharmacol. 41, 240-255) have recently applied dose-time-response models to longitudinal or time-course neurotoxicity data, and have illustrated the modeling process using continuous data from a functional observational battery (FOB). Following the work of these authors, the purpose of this paper is to show that the benchmark dose (BMD) method for single time point dose-response data can be generalized and applied to longitudinal data such as those generated in neurotoxicity studies. We propose a statistical procedure called bootstrap method for computing the lower confidence limits for the BMD. We demonstrate the method using three previously published FOB datasets of triethyltin (Moser, V.C., Becking, G.C., Cuomo, V., Frantik, E., Kulig, B., MacPhail, R.C., Tilson, H.A., Winneke, G., Brightwell, W.S., DeSalvia, M.A., Gill, M.W., Haggerty, G.C., Hornychova, M., Lammers, J., Larsson, J., McDaniel, K.L., Nelson, B.K., Ostergaard, G., 1997a. The IPCS study on neurobehavioral screening methods: results of chemical testing. Neurotoxicology 18, 969-1056.) and the models of Zhu et al. (Zhu, Y., Wessel, M., Liu, T., Moser, V.C., 2005. Analyses of neurobehavioral screening data: dose-time-response modeling of continuous outcomes. Regul. Toxicol. Pharmacol. 41, 240-255).
[Mh] Termos MeSH primário: Algoritmos
Comportamento Animal/efeitos dos fármacos
Intoxicação do Sistema Nervoso por Metais Pesados/fisiopatologia
Compostos de Trietilestanho/toxicidade
[Mh] Termos MeSH secundário: Animais
Benchmarking/métodos
Benchmarking/estatística & dados numéricos
Relação Dose-Resposta a Droga
Membro Anterior/efeitos dos fármacos
Membro Anterior/fisiopatologia
Intoxicação do Sistema Nervoso por Metais Pesados/etiologia
Membro Posterior/efeitos dos fármacos
Membro Posterior/fisiopatologia
Modelos Biológicos
Ratos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Triethyltin Compounds); 5XCT3EQJ85 (triethyltin)
[Em] Mês de entrada:0605
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050505
[St] Status:MEDLINE


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[PMID]:15375695
[Au] Autor:Takahashi T; Hatamoto O; Koyama Y; Abe K
[Ad] Endereço:Research and Development Division, Kikkoman Corporation, 399 Noda, 278-0037 Noda City, Chiba, Japan. ttakahashi@mail.kikkoman.co.jp
[Ti] Título:Efficient gene disruption in the koji-mold Aspergillus sojae using a novel variation of the positive-negative method.
[So] Source:Mol Genet Genomics;272(3):344-52, 2004 Oct.
[Is] ISSN:1617-4615
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:When no phenotypic screen is available, gene disruption in the koji-mold Aspergillus sojae is a time-consuming process, owing to the low frequency of homologous recombination. To achieve efficient gene disruption in the koji-mold, we developed a novel positive-negative selection method to enrich for homologous recombinants. The pyrG gene from A. sojae was used as a positive selection marker for transformants, and the oliC31 gene of A. nidulans, which codes for a mutant form of subunit 9 of the F1FO-ATPase, was employed as a negative selection marker to facilitate elimination of non-homologous recombinants among the transformants. The positive-negative selection markers, in combination with a pyrG deletion strain as a host, enabled enrichment for homologous recombinants, and disruption of the genes niaD, areA and tannase was successfully demonstrated. In order to examine whether the positive-negative selection technique is effective for targeting any locus, even in the absence of information on gene function or phenotype, we attempted to disrupt the aflR gene of A. sojae, which codes for a putative transcription factor for the aflatoxin biosynthetic pathway, using the method. Despite the fact that this gene is not transcribed in A. sojae, aflR disruptants were efficiently obtained, suggesting that the method is indeed capable of targeting any locus, without additional ectopic integration, and is thus applicable for functional genomics studies in filamentous fungi, including A. sojae.
[Mh] Termos MeSH primário: Aspergillus/genética
Genes Fúngicos
Variação Genética
[Mh] Termos MeSH secundário: Sequência de Bases
Meios de Cultura
Primers do DNA
Vetores Genéticos
Compostos de Trietilestanho/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); 0 (DNA Primers); 0 (Triethyltin Compounds); 5XCT3EQJ85 (triethyltin)
[Em] Mês de entrada:0412
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040918
[St] Status:MEDLINE


  7 / 221 MEDLINE  
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[PMID]:15294345
[Au] Autor:Cristòfol RM; Gassó S; Vílchez D; Pertusa M; Rodríguez-Farré E; Sanfeliu C
[Ad] Endereço:Department of Pharmacology and Toxicology, Institut d'Investigacions Biomèdiques de Barcelona, CSIC, IDIBAPS, Rosselló 161, Barcelona E-08034, Spain. rcmfat@iibb.csic.es
[Ti] Título:Neurotoxic effects of trimethyltin and triethyltin on human fetal neuron and astrocyte cultures: a comparative study with rat neuronal cultures and human cell lines.
[So] Source:Toxicol Lett;152(1):35-46, 2004 Aug 30.
[Is] ISSN:0378-4274
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Trimethyltin (TMT) and triethyltin (TET) caused cell death in cultures of primary human neurons and astrocytes, rat neurons and human neuroblastoma cell lines. Human neurons and astrocytes showed a delayed response to TMT cytotoxicity. After 24h of TMT exposure, LC50 values were 148.1, 335.5 and 609.7 microM for SK-N-MC neuroblastoma cell line, neurons and astrocytes, respectively. Over 5 days of exposure, the cytotoxic potency of TMT increased about 70-fold in human cortical neurons. Rat hippocampal neurons were the most vulnerable cells to TMT cytotoxicity, exhibiting an LC50 value 30-fold lower (1.4 microM) than that of rat cerebellar granule cells (44.28 microM). With the exception of rat hippocampal neurons, TET was more potent than TMT in inducing cell death (LC50 values of 3.5-16.9 microM). Moreover, TET was more effective than TMT in increasing intracellular free Ca2+ concentration in human and rat neurons. This work shows that human fetal neuron and astrocyte cultures are a useful model for studying the neurotoxic effects of these environmental contaminants and, thus, predicting their impact on human health.
[Mh] Termos MeSH primário: Astrócitos/efeitos dos fármacos
Astrócitos/patologia
Neurônios/efeitos dos fármacos
Neurônios/patologia
Compostos de Trietilestanho/toxicidade
Compostos de Trimetilestanho/toxicidade
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Linhagem Celular
Feto/citologia
Seres Humanos
Masculino
Neuroblastoma/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Triethyltin Compounds); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin); 5XCT3EQJ85 (triethyltin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0410
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040806
[St] Status:MEDLINE


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[PMID]:15048856
[Au] Autor:Stahnke T; Richter-Landsberg C
[Ad] Endereço:Department of Biology, Molecular Biology, University of Oldenburg, Oldenburg, Germany.
[Ti] Título:Triethyltin-induced stress responses and apoptotic cell death in cultured oligodendrocytes.
[So] Source:Glia;46(3):334-44, 2004 May.
[Is] ISSN:0894-1491
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Triethyltin (TET)-induced neurotoxicity in the brain causes the formation of myelin edema and loss. Myelin deficits produced by early postnatal exposure to TET are permanent and cannot be repaired as the brain matures. The underlying causes have not been resolved. To investigate whether TET directly affects oligodendrocytes, the myelin-forming cells of the central nervous system, cultured rat brain oligodendrocytes were prepared and treated with TET. The data show that TET was cytotoxic for oligodendrocytes and led to the onset of programmed cell death, as indicated by DNA fragmentation. Cellular membranous extensions were severely damaged, and the nuclei appeared to be condensed and fragmented. Concomitantly, the small heat shock protein HSP32, also known as heme oxygenase-1 (HO-1), and an indicator of oxidative stress, as well as the activation of extracellular signal-regulated kinases 1 and 2 (ERK1,2), were observed. ERK1,2 have been implicated to participate in the regulation of cell death and survival. Myelin-specific proteins MBP and CNP were not affected. In TET-treated cells mitochondria redistributed from the processes to the cell somata near the nucleus, possibly as a consequence of microtubule disorganization. A disturbance of the mitochondrial membrane potential and mitochondrial fragmentation occurred. Hence, it might be hypothesized that oligodendroglial PCD, rather than axonal degeneration, contributes to myelin damage and deficits observed in rats after treatment with TET in vivo.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Oligodendroglia/efeitos dos fármacos
Oligodendroglia/metabolismo
Compostos de Trietilestanho/toxicidade
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Morte Celular/fisiologia
Células Cultivadas
Oligodendroglia/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Triethyltin Compounds); 5XCT3EQJ85 (triethyltin)
[Em] Mês de entrada:0405
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040330
[St] Status:MEDLINE


  9 / 221 MEDLINE  
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Bruzzo, Cristina
[PMID]:12635657
[Au] Autor:Barbieri F; Sparatore F; Bonavia R; Bruzzo C; Schettini G; Alama A
[Ad] Endereço:Laboratory of Pharmacology and Neuroscience, National Institute for Cancer Research, Advanced Biotechnology Center, Genoa, Italy.
[Ti] Título:Chemosensitivity of glioblastoma cells during treatment with the organo-tin compound triethyltin(IV)lupinylsulfide hydrochloride.
[So] Source:J Neurooncol;60(2):109-16, 2002 Nov.
[Is] ISSN:0167-594X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Malignant gliomas are the most common primary brain tumors in humans. However, poor response to conventional therapeutic approaches, including chemotherapy, leads invariably to disease recurrence and progression. The organo-tin derivative triethyltin(IV)lupinylsulfide hydrochloride (IST-FS 29) was identified and developed as potential antiproliferative agent in human cancer cell lines. However, for its peculiar chemical structure and good lipophilicity, this compound also appeared an eligible candidate for the treatment of gliobastoma cells. The present experiments were designed to explore the in vitro effects of IST-FS 29 on four human glioblastoma cell lines: A-172, DBTRG.05MG, U-87MG and CAS-1. The average IC50 values were obtained by MTT assay and ranged between 3 and 10 microM. Time-course assays with cell recovery after drug withdrawal, demonstrated marked cytotoxicity following exposure to IST-FS 29 for 8, 24 and 72 h. Cultures treated for 8 h were able to partially re-grow by 144 h; on the contrary, longer times of exposure did not allow surviving cells to recover from the damage and actively proliferate. Cell morphology of cultures exposed to IST-FS 29 was assessed by inverted light microscopy after 24 and 72 h and was more consistent with cell death by necrosis which included cell size reduction, vacuolation of cytoplasm, round dying cells. The present results and our previous data, in vitro and in vivo, indicate the relevant cytotoxic activity of this organo-tin compound and suggest that IST-FS 29 might be a promising novel agent to be developed for the treatment of malignant brain neoplasms.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias Encefálicas
Glioblastoma
Compostos de Trietilestanho/farmacologia
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Transdução de Sinais/efeitos dos fármacos
Células Tumorais Cultivadas/citologia
Células Tumorais Cultivadas/efeitos dos fármacos
Células Tumorais Cultivadas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (IST-FS 29); 0 (Triethyltin Compounds); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0304
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030315
[St] Status:MEDLINE


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[PMID]:12412640
[Au] Autor:Jiann BP; Chou KJ; Chang HT; Chen WC; Huang JK; Jan CR
[Ad] Endereço:Department of Surgery, Kaohsiung Veterans General Hospital, Taiwan, ROC.
[Ti] Título:Effect of triethyltin on Ca2+ movement in Madin-Darby canine kidney cells.
[So] Source:Hum Exp Toxicol;21(8):457-62, 2002 Aug.
[Is] ISSN:0960-3271
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effects of the environmental toxicant, triethyltin, on Ca2+ mobilization in Madin-Darby canine kidney (MDCK) cells have been examined. Triethyltin induced an increase in cytosolic free Ca2+ levels ([Ca2+]i) at concentrations larger than 2 microM in a concentration-dependent manner. Within 5 min, the [Ca2+]i signal was composed of a gradual rise and a sustained phase. The [Ca2+]i signal was partly reduced by removing extracellular Ca2+. In Ca(2+)-free medium, pretreatment with thapsigargin (1 microM), an endoplasmic reticulum Ca2+ pump inhibitor, reduced 50 microM triethyltin-induced [Ca2+]i increase by 80%. Conversely, pretreatment with triethyltin abolished thapsigargin-induced Ca2+ release. Pretreatment with U73122 (2 microM) to inhibit phospholipase C-coupled inositol 1,4,5-trisphosphate formations failed to alter 50 microM triethyltin-induced Ca2+ release. Incubation with triethyltin at a concentration (1 microM) that did not increase basal [Ca2+]i for 3 min did not alter ATP (10 microM)- and bradykinin (1 microM)-induced [Ca2+]i increases. Collectively, this study shows that triethyltin altered Ca2+ movement in renal tubular cells by releasing Ca2+ from multiple stores in an inositol 1,4,5-trisphosphate-independent manner, and by inducing Ca2+ influx.
[Mh] Termos MeSH primário: Cálcio/farmacocinética
Poluentes Ambientais/farmacologia
Rim/fisiologia
Compostos de Trietilestanho/farmacologia
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Cães
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/farmacologia
Rim/citologia
Transdução de Sinais
Tapsigargina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Enzyme Inhibitors); 0 (Triethyltin Compounds); 5XCT3EQJ85 (triethyltin); 67526-95-8 (Thapsigargin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0304
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:021105
[St] Status:MEDLINE



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