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[PMID]:24779638
[Au] Autor:Mitchell SC; Waring RH; Smith RL
[Ad] Endereço:Computational and Systems Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London , South Kensington, London , UK and.
[Ti] Título:Curiosities in drug metabolism.
[So] Source:Xenobiotica;44(7):666-76, 2014 Jul.
[Is] ISSN:1366-5928
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1. It is inevitable that during some xenobiotic biotransformation studies, a certain metabolite or degradation product arises of which the identity is uncertain, the route of formation is ambiguous, or it is just a plain mystery. 2. The following communication draws attention to three drugs reported in the literature, chlorphentermine, phenothiazine and aminopyrine, where after many years of investigation there still exists uncertainty over some of their metabolites. Noticeably, these three examples probably involve (potential) interaction of a nitrogen centre within the drug molecule. 3. It is hoped that the resurrection and assemblage of these data will offer interesting reading and that these examples may prove sufficiently intriguing to motivate further exploration and some resolution of these lingering concerns.
[Mh] Termos MeSH primário: Aminopirina/farmacocinética
Clorfentermina/farmacocinética
Fenotiazinas/farmacocinética
[Mh] Termos MeSH secundário: Aminopirina/metabolismo
Animais
Clorfentermina/metabolismo
Seres Humanos
Inativação Metabólica
Nitrogênio/química
Fenotiazinas/metabolismo
Xenobióticos/metabolismo
Xenobióticos/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phenothiazines); 0 (Xenobiotics); 01704YP3MO (Aminopyrine); GS9EX7QNU6 (phenothiazine); N762921K75 (Nitrogen); NHW07912O7 (Chlorphentermine)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:140604
[Lr] Data última revisão:
140604
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140501
[St] Status:MEDLINE
[do] DOI:10.3109/00498254.2014.913084


  2 / 291 MEDLINE  
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[PMID]:11204319
[Au] Autor:Czupryniak L; Drzewoski J
[Ti] Título:[The role of pharmacotherapy for treatment of obesity in adults].
[Ti] Título:Znaczenie farmakoterapii w leczeniu otylosci u osób doroslych..
[So] Source:Pol Merkur Lekarski;9(53):741-5, 2000 Nov.
[Is] ISSN:1426-9686
[Cp] País de publicação:Poland
[La] Idioma:pol
[Ab] Resumo:Obesity is one of the pathologies with ever-increasing prevalence in modern societies. Its occurrence is strongly associated with increased risk of developing diabetes mellitus, atherosclerosis, hypertension, stroke, heart and respiratory failure, breast, prostate and gut cancer, gall stones, arthropathy. Obesity is common in Polish population. Obesity treatment is difficult and frustrating. It consists of several parts like diet, increased physical activity, lifestyle changes, drug therapy and surgery. However, obesity treatment is very often a failure, mostly because of discouraging long-term results and the necessity of intensive patient's involvement in the therapy. For many patients and doctors weight-decreasing agents look promising. The groups of anti-obesity drugs are presented in the article, with special reference to serotoninergic agents and intestinal lipase inhibitors. The prospects for new anti-obesity agents are discussed. Nevertheless, despite intensive research on obesity, we are still waiting for the development of an effective and safe drugs helping lose weight.
[Mh] Termos MeSH primário: Fármacos Antiobesidade/uso terapêutico
Obesidade/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Animais
Clorfentermina/uso terapêutico
Ciclobutanos/uso terapêutico
Dexfenfluramina/uso terapêutico
Agonistas de Dopamina/uso terapêutico
Efedrina/uso terapêutico
Fluoxetina/uso terapêutico
Seres Humanos
Lactonas/uso terapêutico
Mazindol/uso terapêutico
[Pt] Tipo de publicação:EDITORIAL; ENGLISH ABSTRACT
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 0 (Cyclobutanes); 0 (Dopamine Agonists); 0 (Lactones); 01K63SUP8D (Fluoxetine); 95M8R751W8 (orlistat); C56709M5NH (Mazindol); E35R3G56OV (Dexfenfluramine); GN83C131XS (Ephedrine); NHW07912O7 (Chlorphentermine); WV5EC51866 (sibutramine)
[Em] Mês de entrada:0103
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:010224
[St] Status:MEDLINE


  3 / 291 MEDLINE  
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[PMID]:10767057
[Au] Autor:Baumann MH; Ayestas MA; Dersch CM; Brockington A; Rice KC; Rothman RB
[Ad] Endereço:Clinical Psychopharmacology Section, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland 21224, USA.
[Ti] Título:Effects of phentermine and fenfluramine on extracellular dopamine and serotonin in rat nucleus accumbens: therapeutic implications.
[So] Source:Synapse;36(2):102-13, 2000 May.
[Is] ISSN:0887-4476
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Combined administration of the amphetamine analogs phentermine and fenfluramine (PHEN/FEN) has been used in the treatment of obesity. While these medications are thought to modulate monoamine transmission, the precise neurochemical effects of the PHEN/FEN mixture have not been extensively studied. To assess the mechanism of PHEN/FEN action, in vivo microdialysis studies were performed in the nucleus accumbens of conscious freely moving rats. A series of amphetamine derivatives including phentermine, chlorphentermine, fenfluramine, and PHEN/FEN (1:1 ratio), were infused locally into the accumbens via reverse-dialysis (1, 10, 100 microM) or injected systemically (1 mg/kg, ip). Dialysate samples were assayed for dopamine (DA) and serotonin (5-HT) by high-performance liquid chromatography with electrochemical detection. When infused locally, phentermine preferentially increased extracellular DA, whereas fenfluramine selectively increased extracellular 5-HT. Local administration of chlorphentermine or the PHEN/FEN mixture caused parallel elevations of both transmitters. Analogous results were obtained when the drugs were injected systemically. Phentermine stimulated robust locomotor activity in mice, whereas chlorphentermine and fenfluramine did not. PHEN/FEN caused modest locomotor stimulation after a low dose, but had no effect at the highest dose. Accumulating evidence suggests that chronic drug and alcohol abuse is associated with deficits in both DA and 5-HT neuronal function. Thus, dual activation of DA and 5-HT neurotransmission with monoamine releasing agents may be an effective treatment strategy for substance use disorders, as well as for obesity. Synapse 36:102-113, 2000. Published 2000 Wiley-Liss, Inc.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Espaço Extracelular/efeitos dos fármacos
Espaço Extracelular/metabolismo
Fenfluramina/farmacologia
Núcleo Accumbens/efeitos dos fármacos
Núcleo Accumbens/metabolismo
Fentermina/farmacologia
Inibidores da Captação de Serotonina/farmacologia
Serotonina/metabolismo
Simpatomiméticos/farmacologia
[Mh] Termos MeSH secundário: Anfetamina/farmacologia
Animais
Clorfentermina/farmacologia
Cocaína/análogos & derivados
Cocaína/farmacologia
Técnicas In Vitro
Radioisótopos do Iodo
Masculino
Microdiálise
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Núcleo Accumbens/citologia
Ensaio Radioligante
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Iodine Radioisotopes); 0 (Serotonin Uptake Inhibitors); 0 (Sympathomimetics); 2DS058H2CF (Fenfluramine); 333DO1RDJY (Serotonin); 4H1Z7121WS (2beta-carbomethoxy-3beta-(4-iodophenyl)tropane); C045TQL4WP (Phentermine); CK833KGX7E (Amphetamine); I5Y540LHVR (Cocaine); NHW07912O7 (Chlorphentermine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:0005
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:000415
[St] Status:MEDLINE


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[PMID]:10716603
[Au] Autor:Valodia P; Syce JA
[Ad] Endereço:Department of Pharmacology, University of the Western Cape, Bellville, South Africa.
[Ti] Título:The effect of fenfluramine on the pulmonary disposition of 5-hydroxytryptamine in the isolated perfused rat lung: a comparison with chlorphentermine.
[So] Source:J Pharm Pharmacol;52(1):53-8, 2000 Jan.
[Is] ISSN:0022-3573
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A possible mechanism for fenfluramine-induced pulmonary hypertension has been investigated. Fenfluramine, like chlorphentermine, may inhibit the pulmonary uptake and/or metabolism of 5-hydroxytryptamine (5-HT). This allows more 5-HT to remain in the pulmonary circulation, where it may exert a greater vasoconstrictor action resulting in pulmonary hypertension. Chlorphentermine has been shown to inhibit the uptake and metabolism of 5-HT. The effect of fenfluramine on the pulmonary disposition of [14C]5-HT has been investigated, in comparison with chlorphentermine, using a recirculating isolated perfused rat lung system. The pulmonary disposition of [14C]5-HT was assessed by measuring the change in [14C]5-HT concentration in the perfusion medium during the experiment and at the end, and the concentration in the lung at the end of the experiment. The concentration of 5-hydroxyindoleacetic acid, a metabolite of 5-HT, was measured in perfusate and lung samples. Mean pulmonary clearance of 5-HT for the control lung and lungs challenged with either fenfluramine (2.5 microM) or chlorphentermine (25 microM) was 4.514, 1.316 and 1.007 mL min(-1), respectively (n = 5). The concentration of 5-HT found in the lungs at the end of the experiment for the control and the lungs preloaded with fenfluramine or chlorphentermine was 695.05+/-9.69, 638.65+/-10.27 and 617.3+/-14.38 ng g(-1), respectively. Fenfluramine, like chlorphentermine, inhibited the pulmonary disposition of 5-HT resulting in an elevated perfusate level of 5-HT. This is a possible contributing mechanism for fenfluramine-induced pulmonary hypertension. The effect of fenfluramine was less pronounced than chlorphentermine.
[Mh] Termos MeSH primário: Clorfentermina/farmacologia
Fenfluramina/farmacologia
Depuradores de Radicais Livres/metabolismo
Pulmão/efeitos dos fármacos
Inibidores da Captação de Serotonina/farmacologia
Serotonina/metabolismo
Simpatomiméticos/farmacologia
[Mh] Termos MeSH secundário: Animais
Cromatografia Líquida
Feminino
Depuradores de Radicais Livres/análise
Ácido Hidroxi-Indolacético/análise
Ácido Hidroxi-Indolacético/metabolismo
Pulmão/metabolismo
Taxa de Depuração Metabólica/efeitos dos fármacos
Perfusão
Ratos
Serotonina/análise
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Free Radical Scavengers); 0 (Serotonin Uptake Inhibitors); 0 (Sympathomimetics); 2DS058H2CF (Fenfluramine); 333DO1RDJY (Serotonin); 54-16-0 (Hydroxyindoleacetic Acid); NHW07912O7 (Chlorphentermine)
[Em] Mês de entrada:0004
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:000315
[St] Status:MEDLINE


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[PMID]:10458725
[Au] Autor:Rothman RB; Ayestas MA; Dersch CM; Baumann MH
[Ad] Endereço:Clinical Psychopharmacology Section, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, Md, USA. rrothman@intra.nida.nih.gov
[Ti] Título:Aminorex, fenfluramine, and chlorphentermine are serotonin transporter substrates. Implications for primary pulmonary hypertension.
[So] Source:Circulation;100(8):869-75, 1999 Aug 24.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Coadministration of phentermine and fenfluramine (phen/fen) effectively treats obesity and possibly addictive disorders. The association of fenfluramine and certain other anorexic agents with serious side effects, such as cardiac valvulopathy and primary pulmonary hypertension (PPH), limits the clinical utility of these drugs. Development of new medications that produce neurochemical effects like phen/fen without causing unwanted side effects would be a significant therapeutic breakthrough. METHODS AND RESULTS: We tested the hypothesis that fenfluramine (and other anorexic agents) might increase the risk of PPH through interactions with serotonin (5-HT) transporters. Because 5-HT transporter proteins in the lung and brain are identical, we examined, in rat brain, the effects of selected drugs on 5-HT efflux in vivo and monoamine transporters in vitro as a generalized index of transporter function. Our data show that drugs known or suspected to increase the risk of PPH (eg, aminorex, fenfluramine, and chlorphentermine) are 5-HT transporter substrates, whereas drugs that have not been shown to increase the risk of PPH are less potent in this regard. CONCLUSIONS: We speculate that medications that are 5-HT transporter substrates get translocated into pulmonary cells where, depending on the degree of drug retention, their intrinsic drug toxicity, and individual susceptibility, PPH could develop as a response to high levels of these drugs or metabolites. Emerging evidence suggests that it is possible to develop transporter substrates devoid of adverse side effects. Such medications could have therapeutic application in the management of obesity, drug dependence, depression, and other disorders.
[Mh] Termos MeSH primário: Aminorex/metabolismo
Depressores do Apetite/metabolismo
Proteínas de Transporte/metabolismo
Clorfentermina/metabolismo
Fenfluramina/metabolismo
Hipertensão Pulmonar/induzido quimicamente
Glicoproteínas de Membrana/metabolismo
Proteínas de Membrana Transportadoras
Proteínas do Tecido Nervoso
Serotonina/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Dopamina/metabolismo
Masculino
Microdiálise
Ratos
Ratos Sprague-Dawley
Proteínas da Membrana Plasmática de Transporte de Serotonina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Appetite Depressants); 0 (Carrier Proteins); 0 (Membrane Glycoproteins); 0 (Membrane Transport Proteins); 0 (Nerve Tissue Proteins); 0 (Serotonin Plasma Membrane Transport Proteins); 0 (Slc6a4 protein, rat); 2DS058H2CF (Fenfluramine); 2SH16612I9 (Aminorex); 333DO1RDJY (Serotonin); NHW07912O7 (Chlorphentermine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:9909
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:990824
[St] Status:MEDLINE


  6 / 291 MEDLINE  
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[PMID]:10220731
[Au] Autor:Bredehorn T; Duncker GI
[Ad] Endereço:Klinik und Poliklinik für Augenheilkunde der Martin-Luther-Universität Halle-Wittenberg.
[Ti] Título:[Chloroquine- and chlorphentermin-induced lipidosis in rat retina].
[Ti] Título:Chloroquin und Chlorphentermin induzierte Lipidose der Rattenretina..
[So] Source:Klin Monbl Augenheilkd;214(3):178-82, 1999 Mar.
[Is] ISSN:0023-2165
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:BACKGROUND: The amphiphilic drugs chloroquine and chlorphentermine are known to cause lipidosis in the human and rat retina. METHODS: We treated femal albino Wistar rats orally with chloroquine for 12 weeks, followed by a period of 4 months with normal feed and another group with chlorphentermine for 4-16 weeks. The animals were submitted to electroretinography, and the retinae were prepared for histological investigations. RESULTS: Chloroquine caused severe lipidosis in the neuroretina and slight photoreceptor cell degeneration after 12 weeks of treatment. The b-wave was reduced to 30% of initial values. After withdrawal the lipidosis remitted, but the degeneration of the photoreceptor cell layer continued to progress. The a-wave and b-wave amplitudes were reduced to 25% and 16% of initial values, respectively. Chlorphentermine caused pronounced lipidosis in the pigment epithelium and less numerous in the neuroretina after 16 weeks; no photoreceptor cell degeneration was found. The b-wave was reduced to 80% of initial values, the a-wave appeared unaffected. CONCLUSION: Whether lipidosis is the primary cause of changes in the electroretinogram and of receptor cell degeneration is doubtful. Excessive lipid storage may be the cause of secondary changes. It is unlikely that lipidosis in pigment epithelium played a role.
[Mh] Termos MeSH primário: Cloroquina/farmacologia
Clorfentermina/farmacologia
Lipidoses/induzido quimicamente
Retina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração Oral
Animais
Relação Dose-Resposta a Droga
Eletrorretinografia
Feminino
Ratos
Ratos Wistar
Retina/patologia
Células Fotorreceptoras Retinianas Cones/efeitos dos fármacos
Células Fotorreceptoras Retinianas Cones/patologia
Fatores de Tempo
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
886U3H6UFF (Chloroquine); NHW07912O7 (Chlorphentermine)
[Em] Mês de entrada:9907
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:990430
[St] Status:MEDLINE


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[PMID]:8968411
[Au] Autor:Miles PR; Bowman L; Reasor MJ
[Ad] Endereço:Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Morgantown, West Virginia, USA.
[Ti] Título:Exposure to crystalline silica or treatment with chlorphentermine increases vitamin E levels in rat alveolar lavage materials.
[So] Source:J Toxicol Environ Health;49(5):511-23, 1996 Dec 06.
[Is] ISSN:0098-4108
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that vitamin E may be an integral part of lung surfactant and may function to protect this material from oxidant damage. Therefore, we measured the vitamin E levels in alveolar lavage materials from rats exposed to crystalline silica or treated with chlorphentermine (CP), two treatments that are known to increase surfactant phospholipids (PL) by different mechanisms. Silica exposure leads to increased PL synthesis, and CP treatment causes a reduction in PL degradation. Two different silica preparations, HCL-washed and unwashed silica, were used because exposure to each of them leads to different degrees of phospholipidosis. Exposure to HCL-washed silica results in a more than 17-fold increase in lavage PL and protein levels and a 12.2-fold increase in the amount of vitamin E. Exposure to unwashed silica leads to an approximately 7-fold increase in PL and proteins and a 5.8-fold increase in lavage vitamin E. Following treatment of rats with CP, there is a 15- to 19-fold increase in lavage PL and proteins and a 13.6-fold increase in vitamin E. When the results are expressed as micrograms vitamin E per milligram of lavage PL or protein, there is not much difference between controls and each treatment group. Because surfactant synthesis occurs in the endoplasmic reticulum, we also measured vitamin E in lung microsomes. Both silica exposure and CP treatment also lead to 1.8- to 2.5-fold increases, respectively, in the lung microsomal levels of vitamin E. These results demonstrate that alveolar lavage vitamin E levels are elevated along with lavage PL and proteins, and lung microsomal vitamin E levels are increased following exposure of rats to silica or treatment of the animals with CP.
[Mh] Termos MeSH primário: Líquido da Lavagem Broncoalveolar/química
Clorfentermina/toxicidade
Microssomos Hepáticos/metabolismo
Fosfolipídeos/secreção
Dióxido de Silício/toxicidade
Simpatomiméticos/toxicidade
Vitamina E/secreção
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Clorfentermina/administração & dosagem
Injeções Intraperitoneais
Intubação Intratraqueal
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Masculino
Microssomos Hepáticos/química
Tamanho do Órgão/efeitos dos fármacos
Surfactantes Pulmonares/química
Surfactantes Pulmonares/metabolismo
Ratos
Ratos Sprague-Dawley
Dióxido de Silício/administração & dosagem
Simpatomiméticos/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phospholipids); 0 (Pulmonary Surfactants); 0 (Sympathomimetics); 1406-18-4 (Vitamin E); 7631-86-9 (Silicon Dioxide); NHW07912O7 (Chlorphentermine)
[Em] Mês de entrada:9701
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:961206
[St] Status:MEDLINE


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[PMID]:7871542
[Au] Autor:Waites CR; Bugelski PJ; Badger AM
[Ad] Endereço:Department of Toxicology, SmithKline Beecham Pharmaceuticals, King of Prussia, Pennsylvania 19406.
[Ti] Título:Biochemical and functional analysis of rat bronchoalveolar macrophages containing chemically induced phospholipid inclusions.
[So] Source:Toxicol Appl Pharmacol;130(2):316-21, 1995 Feb.
[Is] ISSN:0041-008X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cationic amphiphilic drugs (CADs) are structurally characterized by hydrophobic ring structures and hydrophilic side chains. Studies have demonstrated that repeated administration of CADs to experimental animals and humans may induce phospholipid (PL) accumulation within the cells of various tissues. The immunomodulatory azaspiranes are novel CADs with beneficial effects in a number of animal models of autoimmune disease and transplantation. Although the mechanism of action of these compounds is unclear, efficacy in all of the disease models is accompanied by the generation of suppressor cell (SC) activity in various lymphoid organs. SK&F 105685 (N,N-dimethyl-8,8-dipropyl-2-azaspiro[4,5]decane-2-propanamine+ ++ hydrochloride) and two analogs, SK&F 106615 and SK&F 103811, were compared with chlorphentermine and chloroquine for their ability to induce PL accumulation and SC activity. Oral administration of SK&F 105685 and SK&F 106615 caused PL accumulation in bronchoalveolar lavage macrophages (AM) but to a far lesser extent (three- to fivefold) than chlorphentermine. Neither the immunologically unreactive azaspirane SK&F 103811 nor chloroquine affected PL levels. AM from rats treated with SK&F 105685 or SK&F 106615 expressed more potent SC activity than chlorphentermine. Thus, SC activity did not correlate with the extent of PL accumulation. Neither SK&F 103811 nor chloroquine induced SC activity. AM from SK&F 105685-treated rats had an enhanced ability to kill the opportunistic pathogen Candida albicans in vitro indicating that there was no impairment of macrophage-dependent host defense mechanisms.
[Mh] Termos MeSH primário: Brônquios/metabolismo
Macrófagos Alveolares/metabolismo
Fosfolipídeos/metabolismo
Compostos de Espiro/farmacologia
[Mh] Termos MeSH secundário: Animais
Brônquios/efeitos dos fármacos
Candida albicans/efeitos dos fármacos
Cloroquina/farmacologia
Clorfentermina/farmacologia
Imunossupressores/farmacologia
Corpos de Inclusão/metabolismo
Macrófagos Alveolares/efeitos dos fármacos
Masculino
Alvéolos Pulmonares/efeitos dos fármacos
Alvéolos Pulmonares/metabolismo
Ratos
Ratos Endogâmicos Lew
Relação Estrutura-Atividade
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunosuppressive Agents); 0 (Phospholipids); 0 (Spiro Compounds); 123018-34-8 (SK&F 105685); 886U3H6UFF (Chloroquine); NHW07912O7 (Chlorphentermine)
[Em] Mês de entrada:9503
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950201
[St] Status:MEDLINE


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[PMID]:7556587
[Au] Autor:McCloud CM; Beard TL; Kacew S; Reasor MJ
[Ad] Endereço:Department of Pharmacology and Toxicology, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, USA.
[Ti] Título:In vivo and in vitro reversibility of chlorphentermine-induced phospholipidosis in rat alveolar macrophages.
[So] Source:Exp Mol Pathol;62(1):12-21, 1995 Feb.
[Is] ISSN:0014-4800
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chlorphentermine (CP) is a cationic, amphiphilic drug (CAD) that has been studied widely for its ability to induce phospholipidosis, a disorder characterized by excessive accumulation of cellular phospholipid and ultrastructural development of lysosomal lamellar bodies (LLBs) in the cell. The accumulation of inducing drug correlates with increasing phospholipids. In the present study, we examined the reversibility of this disorder in rat alveolar macrophages (AMs) following a 7-day treatment (30 mg/kg/day, ip). The reversibility of phospholipidosis was examined under in vivo conditions and under in vitro conditions in cell cultures for a period of up to 12 days. There was a marked reduction in cellular CP levels and phospholipid content after 4 days of recovery, both in vivo and in vitro; however, there was no indication of significant loss of LLBs. Beyond this time point, ultrastructural recovery from phospholipidosis lagged behind the biochemical recovery temporally and was somewhat less rapid in vitro than in vivo. By 12 days of recovery, AMs from both groups had recovered biochemically, but a moderate level of LLBs was still present in some AMs in the in vitro recovery group. The results of this study indicate that there are more similarities than differences when comparing the recovery of phospholipidotic cells in vitro to that occurring in vivo. We conclude that the use of cell cultures may prove valuable in studying the reversibility of CAD-induced phospholipidosis.
[Mh] Termos MeSH primário: Clorfentermina/toxicidade
Lipidoses/patologia
Macrófagos Alveolares/química
Fosfolipídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Clorfentermina/análise
Lipidoses/induzido quimicamente
Lisossomos/efeitos dos fármacos
Lisossomos/patologia
Macrófagos Alveolares/ultraestrutura
Masculino
Fosfolipídeos/análise
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phospholipids); NHW07912O7 (Chlorphentermine)
[Em] Mês de entrada:9511
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950201
[St] Status:MEDLINE


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[PMID]:8304588
[Au] Autor:Geist SH; Lüllmann-Rauch R
[Ad] Endereço:Department of Anatomy, University of Kiel, Germany.
[Ti] Título:Experimentally induced lipidosis in uterine and vaginal epithelium of rats.
[So] Source:Ann Anat;176(1):3-9, 1994 Jan.
[Is] ISSN:0940-9602
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to investigate the effects of two lipidosis-inducing drugs (the anorectic drug chlorphentermine and the tricyclic antidepressant-imipramine) upon the estrous cycle of rats and upon the morphology of the vaginal and uterine epithelia. After two weeks of continuous administration of high daily drug doses, the estrous cycle became stagnant. Ultrastructurally, the vaginal and uterine epithelia contained storage lysosomes which were filled with undigested polar lipids appearing as multilamellated material. The uterine luminal epithelium was most severely affected. The estrous cycle was abolished also by treatment with the anorexigenic drug phentermine, although this compound does not cause lipidosis. Therefore, the cessation of the estrous cycle cannot be attributed to the lipidosis as induced by chlorphentermine and imipramine; probably it is a consequence of the main actions of these psychotropic drugs. The biological basis for the exceedingly severe lipidosis in the uterine luminal epithelium is suggested to be the heavy load of polar lipids physiologically delivered to the lysosomal apparatus as long as the cycle-dependent apoptotic and autophagic processes were going on during the early period of drug treatment.
[Mh] Termos MeSH primário: Lipidoses/patologia
Útero/patologia
Vagina/patologia
[Mh] Termos MeSH secundário: Animais
Clorfentermina/toxicidade
Relação Dose-Resposta a Droga
Epitélio/efeitos dos fármacos
Epitélio/patologia
Epitélio/ultraestrutura
Estro/efeitos dos fármacos
Feminino
Imipramina/toxicidade
Lipidoses/induzido quimicamente
Lisossomos/efeitos dos fármacos
Lisossomos/ultraestrutura
Microscopia Eletrônica
Ratos
Ratos Wistar
Útero/efeitos dos fármacos
Útero/ultraestrutura
Vagina/efeitos dos fármacos
Vagina/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
NHW07912O7 (Chlorphentermine); OGG85SX4E4 (Imipramine)
[Em] Mês de entrada:9403
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:940101
[St] Status:MEDLINE



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