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Pesquisa : D03.633.100.473.725 [Categoria DeCS]
Referências encontradas : 61 [refinar]
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[PMID]:24403234
[Au] Autor:Morrison BL; Mullendore ME; Stockwin LH; Borgel S; Hollingshead MG; Newton DL
[Ad] Endereço:Drug Mechanism Group, Biological Testing Branch, Developmental Therapeutics Program, SAIC-Frederick Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland, 21702.
[Ti] Título:Oxyphenisatin acetate (NSC 59687) triggers a cell starvation response leading to autophagy, mitochondrial dysfunction, and autocrine TNFα-mediated apoptosis.
[So] Source:Cancer Med;2(5):687-700, 2013 Oct.
[Is] ISSN:2045-7634
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxyphenisatin (3,3-bis(4-hydroxyphenyl)-1H-indol-2-one) and several structurally related molecules have been shown to have in vitro and in vivo antiproliferative activity. This study aims to confirm and extend mechanistic studies by focusing on oxyphenisatin acetate (OXY, NSC 59687), the pro-drug of oxyphenisatin. Results confirm that OXY inhibits the growth of the breast cancer cell lines MCF7, T47D, HS578T, and MDA-MB-468. This effect is associated with selective inhibition of translation accompanied by rapid phosphorylation of the nutrient sensing eukaryotic translation initiation factor 2α (eIF2α) kinases, GCN2 and PERK. This effect was paralleled by activation of AMP-activated protein kinase (AMPK) combined with reduced phosphorylation of the mammalian target of rapamycin (mTOR) substrates p70S6K and 4E-BP1. Microarray analysis highlighted activation of pathways involved in apoptosis induction, autophagy, RNA/protein metabolism, starvation responses, and solute transport. Pathway inhibitor combination studies suggested a role for AMPK/mTOR signaling, de novo transcription and translation, reactive oxygen species (ROS)/glutathione metabolism, calcium homeostasis and plasma membrane Na(+) /K(+) /Ca(2+) transport in activity. Further examination confirmed that OXY treatment was associated with autophagy, mitochondrial dysfunction, and ROS generation. Additionally, treatment was associated with activation of both intrinsic and extrinsic apoptotic pathways. In the estrogen receptor (ER) positive MCF7 and T47D cells, OXY induced TNFα expression and TNFR1 degradation, indicating autocrine receptor-mediated apoptosis in these lines. Lastly, in an MCF7 xenograft model, OXY delivered intraperitoneally inhibited tumor growth, accompanied by phosphorylation of eIF2α and degradation of TNFR1. These data suggest that OXY induces a multifaceted cell starvation response, which ultimately induces programmed cell death.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Neoplasias da Mama/patologia
Mitocôndrias/efeitos dos fármacos
Acetato de Oxifenisatina/farmacologia
[Mh] Termos MeSH secundário: Animais
Comunicação Autócrina/efeitos dos fármacos
Neoplasias da Mama/metabolismo
Proliferação Celular/efeitos dos fármacos
Avaliação Pré-Clínica de Medicamentos/métodos
Feminino
Seres Humanos
Neoplasias Mamárias Experimentais/metabolismo
Neoplasias Mamárias Experimentais/patologia
Camundongos
Camundongos Nus
Mitocôndrias/fisiologia
Proteínas de Neoplasias/metabolismo
Fosforilação/efeitos dos fármacos
Biossíntese de Proteínas/efeitos dos fármacos
Proteínas Serina-Treonina Quinases/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Análise Serial de Tecidos/métodos
Células Tumorais Cultivadas
Fator de Necrose Tumoral alfa/fisiologia
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Tnfrsf1a protein, mouse); 0 (Tumor Necrosis Factor-alpha); EC 2.7.11.1 (Eif2ak4 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (eIF2alpha kinase, mouse); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:161203
[Lr] Data última revisão:
161203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140110
[St] Status:MEDLINE
[do] DOI:10.1002/cam4.107


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[PMID]:20852860
[Au] Autor:Trojel-Hansen C; Erichsen KD; Christensen MK; Jensen PB; Sehested M; Nielsen SJ
[Ad] Endereço:XPU Bartholin, Rigshospitalet 3731, TopoTarget A/S, Copenhagen Biocenter, Ole Maaløesvej 5, 2200 Copenhagen, Denmark. chh@topotarget.com
[Ti] Título:Novel small molecule drugs inhibit tumor cell metabolism and show potent anti-tumorigenic potential.
[So] Source:Cancer Chemother Pharmacol;68(1):127-38, 2011 Jul.
[Is] ISSN:1432-0843
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Rapidly dividing tumor cells have an increased demand for nutrients to support their characteristic unabated growth; this demand is met by an increased availability of nutrients such as amino acids through vasculogenesis and by the enhanced cellular entry of nutrients through the upregulation of specific transporters. Deprivation of intracellular amino acids or block of amino acid uptake has been shown to be cytotoxic to many established human cancer cell lines in vitro and in human cancer xenograft models. RESULTS: In this paper, we provide evidence that the two small molecule oxyphenisatine analogs TOP001 and TOP216 exert their anti-cancer effect by affecting tumor cell metabolism and inducing intracellular amino acid deprivation, leading to a block of cell proliferation. GCN2-mediated phosphorylation of eIF2α as well as mTOR pathway inhibition supports the above notion. In addition, these novel anti-cancer compounds inhibit DNA and protein synthesis and induce apoptosis in a broad spectrum of cancer cell lines. In vivo, the compounds induce tumor stasis and regression in mouse xenograft models of human breast, prostate, ovarian and pancreatic cancer, both when administered intravenously and orally. CONCLUSION: In conclusion, these small molecules, built on a 1,3-dihydroindole-2-one scaffold, elicit strong anti-proliferative and cytotoxic activity, and importantly, a strong anti-tumorigenicity is observed in in vivo xenograft models of human breast, ovary, prostate and pancreatic cancers encouraging the translation of this class of compounds into the clinic.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Proliferação Celular/efeitos dos fármacos
Neoplasias/tratamento farmacológico
Acetato de Oxifenisatina/análogos & derivados
[Mh] Termos MeSH secundário: Aminoácidos/metabolismo
Animais
Antineoplásicos/química
Apoptose/efeitos dos fármacos
Caspases/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Modelos Animais de Doenças
Metabolismo Energético/efeitos dos fármacos
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Neoplasias/metabolismo
Acetato de Oxifenisatina/química
Acetato de Oxifenisatina/farmacologia
Proteínas Quinases/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Ensaio Tumoral de Célula-Tronco
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Antineoplastic Agents); 0 (Top001 compound); 0 (Top216 compound); EC 2.7.- (Protein Kinases); EC 2.7.1.- (AMP-activated protein kinase kinase); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.1 (mTOR protein, mouse); EC 3.4.22.- (Caspases); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:1108
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100921
[St] Status:MEDLINE
[do] DOI:10.1007/s00280-010-1453-3


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[PMID]:17368900
[Au] Autor:Uddin MK; Reignier SG; Coulter T; Montalbetti C; Grånäs C; Butcher S; Krog-Jensen C; Felding J
[Ad] Endereço:Evotec(UK) Ltd, 111 Milton Park, Abingdon, Oxon OX14 4RX, UK.
[Ti] Título:Syntheses and antiproliferative evaluation of oxyphenisatin derivatives.
[So] Source:Bioorg Med Chem Lett;17(10):2854-7, 2007 May 15.
[Is] ISSN:0960-894X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Syntheses and structure-antiproliferative relationship for oxyphenisatin analogues are described. The cell proliferation data showed that the presence of substituents (especially F, Cl, Me, CF(3), and OMe) in the 6- and 7-position of oxyphenisatin markedly enhanced the potency in the MDA-468 cell line without affecting the MDA-231 cell line. The best compounds from this series showed low nanomolar antiproliferative activity towards the MDA-468 cell line and a 1000-fold selectivity over the MDA-231 cell line.
[Mh] Termos MeSH primário: Antineoplásicos/síntese química
Antineoplásicos/farmacologia
Proliferação Celular/efeitos dos fármacos
Acetato de Oxifenisatina/análogos & derivados
Acetato de Oxifenisatina/síntese química
Acetato de Oxifenisatina/farmacologia
[Mh] Termos MeSH secundário: Seres Humanos
Estrutura Molecular
Relação Estrutura-Atividade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Top001 compound); 0 (Top216 compound); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:0707
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070321
[St] Status:MEDLINE


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[PMID]:3241981
[Au] Autor:Teh LB; Chong R; Ho JM; Ong YY
[Ti] Título:Oxyphenisatin induced chronic active hepatitis--a potential health hazard in Singapore.
[So] Source:Singapore Med J;29(5):508-12, 1988 Oct.
[Is] ISSN:0037-5675
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Mh] Termos MeSH primário: Doença Hepática Crônica Induzida por Substâncias e Drogas
Indóis/efeitos adversos
Acetato de Oxifenisatina/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Constipação Intestinal/tratamento farmacológico
Feminino
Seres Humanos
Acetato de Oxifenisatina/farmacocinética
Singapura
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indoles); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:8905
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:881001
[St] Status:MEDLINE


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[PMID]:6549524
[Au] Autor:Bercetche M; Pérez V; Avaginina A
[Ti] Título:[Chronic hepatitis caused by oxyphenisatin].
[Ti] Título:Hepatitis crónica por oxifenisatina..
[So] Source:Medicina (B Aires);44(1):59-63, 1984.
[Is] ISSN:0025-7680
[Cp] País de publicação:Argentina
[La] Idioma:spa
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/etiologia
Indóis/efeitos adversos
Acetato de Oxifenisatina/efeitos adversos
[Mh] Termos MeSH secundário: Doença Hepática Induzida por Substâncias e Drogas/diagnóstico
Doença Hepática Induzida por Substâncias e Drogas/patologia
Doença Crônica
Feminino
Seres Humanos
Fígado/patologia
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indoles); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:8508
[Cu] Atualização por classe:161123
[Lr] Data última revisão:
161123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:840101
[St] Status:MEDLINE


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[PMID]:6548720
[Au] Autor:Farack UM; Nell G
[Ti] Título:Mechanism of action of diphenolic laxatives: the role of adenylate cyclase and mucosal permeability.
[So] Source:Digestion;30(3):191-4, 1984.
[Is] ISSN:0012-2823
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Net fluid movement and mucosal 14C-erythritol clearance were measured in ligated colonic loops of the rat in vivo. The diphenolic laxatives, oxyphenisatin and bisacodyl, dose-dependently inhibited net fluid absorption or caused secretion, both increased the 14C-erythritol clearance. Pretreatment with the adenylate cyclase inhibitor, RMI 12 330 A, did not change these results. It is concluded that diphenolic laxatives mainly influence intestinal fluid transport not by stimulation of mucosal adenylate cyclase but rather by augmenting epithelial permeability.
[Mh] Termos MeSH primário: Adenilil Ciclases/fisiologia
Catárticos/farmacologia
Permeabilidade da Membrana Celular/efeitos dos fármacos
Mucosa Intestinal/fisiologia
[Mh] Termos MeSH secundário: Inibidores de Adenilil Ciclase
Animais
Bisacodil/farmacologia
Feminino
Iminas/farmacologia
Mucosa Intestinal/efeitos dos fármacos
Acetato de Oxifenisatina/farmacologia
Ratos
Ratos Endogâmicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adenylyl Cyclase Inhibitors); 0 (Cathartics); 0 (Imines); 10X0709Y6I (Bisacodyl); 82985-31-7 (RMI 12330A); EC 4.6.1.1 (Adenylyl Cyclases); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:8412
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:840101
[St] Status:MEDLINE


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[PMID]:6688858
[Au] Autor:Farack UM; Nell G; Rummel W
[Ti] Título:Differentiation of secretagogue drugs by chlorpromazine in rat intestine in vivo.
[So] Source:Naunyn Schmiedebergs Arch Pharmacol;324(1):70-4, 1983 Sep.
[Is] ISSN:0028-1298
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The effect of chlorpromazine (CPZ) on passive epithelial permeability and net fluid movement induced by secretagogues was tested in the rat intestine in vivo. CPZ, in a dose of 20 mg/kg intramuscularly, did not alter colonic permeability either in control conditions or during increased permeability caused by deoxycholic acid (DOC) or bisacodyl. Fluid secretion induced by cholera toxin and theophylline was strongly reduced by CPZ. The effects of oxyphenisatin and bisacodyl were only slightly but significantly inhibited by CPZ, whereas the action of DOC was unaffected. It is concluded, that the increase of the epithelial permeability is the main reason for the augmented fluid secretion caused by DOC. Bisacodyl and oxyphenisatin seem to act partly via an increase in permeability and to some degree via an induction of an active secretory process.
[Mh] Termos MeSH primário: Clorpromazina/farmacologia
Intestinos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Água Corporal/metabolismo
Toxina da Cólera/farmacologia
Ácido Desoxicólico/farmacologia
Feminino
Mucosa Intestinal/secreção
Acetato de Oxifenisatina/farmacologia
Ratos
Ratos Endogâmicos
Teofilina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
005990WHZZ (Deoxycholic Acid); 9012-63-9 (Cholera Toxin); C137DTR5RG (Theophylline); U0Y1YAL65X (Oxyphenisatin Acetate); U42B7VYA4P (Chlorpromazine)
[Em] Mês de entrada:8312
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:830901
[St] Status:MEDLINE


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[PMID]:6982502
[Au] Autor:Døssing M; Andreasen PB
[Ti] Título:Drug-induced liver disease in Denmark. An analysis of 572 cases of hepatotoxicity reported to the Danish Board of Adverse Reactions to Drugs.
[So] Source:Scand J Gastroenterol;17(2):205-11, 1982 Mar.
[Is] ISSN:0036-5521
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During the decade 1968-1978 the Danish Board of Adverse Reactions to Drugs received 572 (6% of the total number) reports on hepatotoxicity. Halothane amounted to one fourth of the reported cases. Among the 94 psychotropic-induced adverse drug reactions 54 cases were attributed to chlorpromazine, 10 to tricyclic antidepressants, and only 2 to benzodiazepines. Considering the drug consumption data, the combination trimethoprim-sulfamethoxazole is nearly five times more frequently associated with hepatotoxicity than administration of sulfamethizole. Almost two thirds of the hepatotoxic reactions were classified as cytotoxic. Halothane, oxyphenisatin, rifampicin, alfa-methyldopa, papaverine, phenytoin, and ajmaline were almost exclusively related to cytotoxic reactions. Excluding the halothane-induced hepatotoxic reactions, the relative mortality of the cytotoxic (6%) reactions is not significantly different from that of the cholestatic (3%) ones. Thirteen percent of the patients with halothane-induced hepatotoxicity died.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/epidemiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Anti-Infecciosos Urinários/efeitos adversos
Antidepressivos Tricíclicos/efeitos adversos
Antituberculosos/efeitos adversos
Benzodiazepinas/efeitos adversos
Criança
Clorpromazina/efeitos adversos
Anticoncepcionais Orais/efeitos adversos
Dinamarca
Combinação de Medicamentos/efeitos adversos
Feminino
Halotano/efeitos adversos
Seres Humanos
Masculino
Meia-Idade
Acetato de Oxifenisatina/efeitos adversos
Gestão de Riscos
Sulfametoxazol/efeitos adversos
Trimetoprima/efeitos adversos
Combinação Trimetoprima e Sulfametoxazol
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents, Urinary); 0 (Antidepressive Agents, Tricyclic); 0 (Antitubercular Agents); 0 (Contraceptives, Oral); 0 (Drug Combinations); 12794-10-4 (Benzodiazepines); 8064-90-2 (Trimethoprim, Sulfamethoxazole Drug Combination); AN164J8Y0X (Trimethoprim); JE42381TNV (Sulfamethoxazole); U0Y1YAL65X (Oxyphenisatin Acetate); U42B7VYA4P (Chlorpromazine); UQT9G45D1P (Halothane)
[Em] Mês de entrada:8212
[Cu] Atualização por classe:161123
[Lr] Data última revisão:
161123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:820301
[St] Status:MEDLINE


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[PMID]:6897480
[Au] Autor:Sund RB; Hillestad B
[Ti] Título:Uptake, conjugation and transport of laxative diphenols by everted sacs of the rat jejunum and stripped colon.
[So] Source:Acta Pharmacol Toxicol (Copenh);51(4):377-87, 1982 Oct.
[Is] ISSN:0001-6683
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Phenolphthalein (PHEN), desacetylbisacodyl (DES) and oxyphenisatin (OXY) were incubated with everted sacs of the rat jejunum and stripped descending colon; the mucosal and serosal fluid were analysed with respect to free and conjugated diphenol by means of HPLC. Conjugates were measured as the amount of free diphenol in completely hydrolyzed samples less the amount before hydrolysis. A study with double-sided administration of PHEN revealed that diphenol uptake from and conjugate output to both sides followed a rectilinear course for 15-90 min. A standard incubation time of 60 min. was chosen for the subsequent experiments, in which the diphenols were administered at the mucosal side at a low and a high concentration. Diphenol uptake, i.e. the amount of free diphenol administered less the amount recovered at the mucosal side, varied in an order (PHEN greater than DES greater than OXY) which seems to be inversely related to the order of water solubility of the compounds. Tissue accumulation and conjugate output relative to uptake varied with the dose, and from one compound to another. At low initial concentration (20 nmol/ml), the compounds were transferred to the jejunal and colonic serosal fluid almost entirely as conjugates (greater than or equal to 95%); the transfer rates followed, qualitatively, the same order as above. In jejunum, more conjugates were released to the mucosal than to the serosal side; in colon the distribution was reversed. Increasing the dose to 100 nmol/ml caused a corresponding increase in uptake, but relative output decreased and tissue accumulation increased; thus demonstrating capacity limitation. With PHEN, the ratio of conjugated:free diphenol on the serosal side remained essentially unchanged; with DES in particular, but also with OXY the ratio decreased. These findings may be interpreted to mean that in case of PHEN capacity limitation is linked to conjugate efflux, while DES and OXY may be poor substrates for glucuronide formation as well. Experiments with serosal side administration like the double-sided PHEN experiments verified the dissimilar conjugate distribution in jejunal and colonic sacs; the phenomenon is to some extent discussed in the text. Identity tests gave evidence that the conjugates were mainly monoglucuronides.
[Mh] Termos MeSH primário: Catárticos/metabolismo
Intestinos/metabolismo
[Mh] Termos MeSH secundário: Animais
Biotransformação
Bisacodil/análogos & derivados
Bisacodil/metabolismo
Colo/metabolismo
Técnicas In Vitro
Mucosa Intestinal/metabolismo
Jejuno/metabolismo
Masculino
Acetato de Oxifenisatina/metabolismo
Fenolftaleínas/metabolismo
Ratos
Ratos Endogâmicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cathartics); 0 (Phenolphthaleins); 10X0709Y6I (Bisacodyl); R09078E41Y (dihydroxydiphenyl-pyridyl methane); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:8302
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:821001
[St] Status:MEDLINE


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[PMID]:6896788
[Au] Autor:Bergan T; Fotland MH; Sund RB
[Ti] Título:Interaction between diphenolic laxatives and intestinal bacteria in vitro.
[So] Source:Acta Pharmacol Toxicol (Copenh);51(2):165-72, 1982 Aug.
[Is] ISSN:0001-6683
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:The ability of the laxative diphenols desacetylbisacodyl, oxyphenisatin, and phenolphthalein to inhibit growth and cause leakage of potassium ion from microbial cells in vitro was studied with 25 aerobic and 25 anaerobic bacterial strains. None of the aerobes, but some of the anaerobes showed growth inhibition. Potassium release assayed by flame photometry was observed in strains which showed growth inhibition, but also in other strains including anaerobes and aerobes. The highest antibacterial activity among the diphenols was observed with phenolphthalein and the least with desacetylbisacodyl; this relationship as noted for both growth inhibition and potassium release. Enzymatic hydrolysis of picosulphate to the free diphenol desacetylbisacodyl carried out by three strains of anaerobic bacteria was indicated by high pressure liquid chromatography.
[Mh] Termos MeSH primário: Bactérias/efeitos dos fármacos
Catárticos/farmacologia
Intestinos/microbiologia
[Mh] Termos MeSH secundário: Bactérias/metabolismo
Bisacodil/análogos & derivados
Bisacodil/farmacologia
Seres Humanos
Acetato de Oxifenisatina/farmacologia
Fenolftaleínas/farmacologia
Potássio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cathartics); 0 (Phenolphthaleins); 10X0709Y6I (Bisacodyl); R09078E41Y (dihydroxydiphenyl-pyridyl methane); RWP5GA015D (Potassium); U0Y1YAL65X (Oxyphenisatin Acetate)
[Em] Mês de entrada:8210
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:820801
[St] Status:MEDLINE



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde