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[PMID]:25726414
[Au] Autor:Miller-Pinsler L; Sharma A; Wells PG
[Ad] Endereço:Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.
[Ti] Título:Enhanced NADPH oxidases and reactive oxygen species in the mechanism of methanol-initiated protein oxidation and embryopathies in vivo and in embryo culture.
[So] Source:Arch Toxicol;90(3):717-30, 2016 Mar.
[Is] ISSN:1432-0738
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Methanol (MeOH) teratogenicity in rodents may be mediated in part by reactive oxygen species (ROS), the source of which is unknown. To determine if MeOH enhances embryonic ROS-producing NADPH oxidases (NOXs), p22phox mRNA and protein and oxidatively damaged protein were measured in gestational day 12 MeOH-exposed CD-1 mouse embryos with or without pretreatment with the free radical spin trap phenylbutylnitrone (PBN) or the NOX inhibitor diphenyleneiodonium chloride (DPI). MeOH exposure upregulated p22phox mRNA and protein expression, and enhanced protein oxidation, within 3-6 h. Compared to embryos exposed to MeOH alone, PBN and DPI pretreatment decreased MeOH-enhanced p22phox mRNA expression, DPI but not PBN blocked p22phox protein expression, and both blocked protein oxidation. To assess developmental relevance, mouse embryos were exposed in culture for 24 h to MeOH or vehicle with or without pretreatment with PBN, DPI, or the prostaglandin H synthase (PHS) inhibitor eicosatetraynoic acid (ETYA), and evaluated for abnormalities. ETYA did not prevent MeOH embryopathies, despite blocking phenytoin embryopathies (ROS-initiating positive control), precluding bioactivation of MeOH or its metabolites by PHS. Concentration-dependent MeOH embryopathies were blocked by both DPI and PBN pretreatment, suggesting that enhanced embryonic NOX-catalyzed ROS formation and oxidative stress may contribute to the mechanism of MeOH embryopathies.
[Mh] Termos MeSH primário: Metanol/toxicidade
NADPH Oxidases/metabolismo
Proteínas/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Animais
Grupo dos Citocromos b/genética
Grupo dos Citocromos b/metabolismo
Relação Dose-Resposta a Droga
Técnicas de Cultura Embrionária
Feminino
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Masculino
Metanol/administração & dosagem
Camundongos Endogâmicos
NADPH Oxidases/genética
Oniocompostos/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytochrome b Group); 0 (Onium Compounds); 0 (Proteins); 0 (Reactive Oxygen Species); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 6HJ411TU98 (diphenyleneiodonium); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.1 (p22(phox) protein, mouse); Y4S76JWI15 (Methanol)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150302
[St] Status:MEDLINE
[do] DOI:10.1007/s00204-015-1482-0


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[PMID]:24699382
[Au] Autor:Kur J; McGahon MK; Fernández JA; Scholfield CN; McGeown JG; Curtis TM
[Ad] Endereço:Centre for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University of Belfast, Northern Ireland, United Kingdom.
[Ti] Título:Role of ion channels and subcellular Ca2+ signaling in arachidonic acid-induced dilation of pressurized retinal arterioles.
[So] Source:Invest Ophthalmol Vis Sci;55(5):2893-902, 2014 May 02.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To investigate the mechanisms responsible for the dilatation of rat retinal arterioles in response to arachidonic acid (AA). METHODS: Changes in the diameter of isolated, pressurized rat retinal arterioles were measured in the presence of AA alone and following pre-incubation with pharmacologic agents inhibiting Ca(2+) sparks and oscillations and K(+) channels. Subcellular Ca(2+) signals were recorded in arteriolar myocytes using Fluo-4-based confocal imaging. The effects of AA on membrane currents of retinal arteriolar myocytes were studied using whole-cell perforated patch clamp recording. RESULTS: Arachidonic acid dilated pressurized retinal arterioles under conditions of myogenic tone. Eicosatetraynoic acid (ETYA) exerted a similar effect, but unlike AA, its effects were rapidly reversible. Arachidonic acid-induced dilation was associated with an inhibition of subcellular Ca(2+) signals. Interventions known to block Ca(2+) sparks and oscillations in retinal arterioles caused dilatation and inhibited AA-induced vasodilator responses. Arachidonic acid accelerated the rate of inactivation of the A-type Kv current and the voltage dependence of inactivation was shifted to more negative membrane potentials. It also enhanced voltage-activated and spontaneous large-conductance calcium-activated K(+) (BK) currents, but only at positive membrane potentials. Pharmacologic inhibition of A-type Kv and BK currents failed to block AA-induced vasodilator responses. Arachidonic acid suppressed L-type Ca(2+) currents. CONCLUSIONS: These results suggest that AA induces retinal arteriolar vasodilation by inhibiting subcellular Ca(2+)-signaling activity in retinal arteriolar myocytes, most likely through a mechanism involving the inhibition of L-type Ca(2+)-channel activity. Arachidonic acid actions on K(+) currents are inconsistent with a model in which K(+) channels contribute to the vasodilator effects of AA.
[Mh] Termos MeSH primário: Ácido Araquidônico/fisiologia
Cálcio/fisiologia
Canais de Potássio/fisiologia
Artéria Retiniana/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Animais
Ácido Araquidônico/farmacologia
Arteríolas/fisiologia
Eletrofisiologia
Modelos Animais
Miócitos de Músculo Liso/efeitos dos fármacos
Canais de Potássio/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Artéria Retiniana/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Vasodilatação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Potassium Channels); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 27YG812J1I (Arachidonic Acid); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140405
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.13-13511


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[PMID]:24012824
[Au] Autor:Di Venere A; Nicolai E; Ivanov I; Dainese E; Adel S; Angelucci BC; Kuhn H; Maccarrone M; Mei G
[Ad] Endereço:Department of Experimental Medicine and Surgery, Tor Vergata University of Rome, Via Montpellier 1, 00133 Rome, Italy.
[Ti] Título:Probing conformational changes in lipoxygenases upon membrane binding: fine-tuning by the active site inhibitor ETYA.
[So] Source:Biochim Biophys Acta;1841(1):1-10, 2014 Jan.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Lipoxygenases (LOXs) are lipid-peroxidizing enzymes that are involved in the metabolism of polyunsaturated fatty acids. Their biological activity includes a membrane binding process whose molecular details are not completely understood. The mechanism of enzyme-membrane interactions is thought to involve conformational changes at the level of the protein tertiary structure, and the extent of such alterations depends on the degree of structural flexibility of the different LOX isoforms. In this study, we have tested the resilience properties of a plant and a mammalian LOX, by using high pressure fluorescence measurements at different temperatures. The binding of LOXs to the lipid bilayer has been characterized using both large and giant unilamellar vesicles and electron transfer particles (inner mitochondrial membranes) as model membranes. The data indicate that the degree of LOXs' flexibility is strictly dependent on the two distinct N- and C-terminal domains that characterize the 3D structure of these enzymes. Furthermore, they demonstrate that increasing the rigidity of protein scaffolding by the presence of an active site ligand impairs the membrane binding ability of LOXs. These findings provide evidence that the amphitropic nature of LOXs is finely tuned by the interaction of the substrate with the residues of the active site, suggesting new strategies for the design of enzyme inhibitors.
[Mh] Termos MeSH primário: Ácido 5,8,11,14-Eicosatetrainoico/química
Bicamadas Lipídicas/química
Inibidores de Lipoxigenase/química
Lipoxigenase/química
Membranas Mitocondriais/química
[Mh] Termos MeSH secundário: Domínio Catalítico
Seres Humanos
Membranas Mitocondriais/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipid Bilayers); 0 (Lipoxygenase Inhibitors); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); EC 1.13.11.12 (Lipoxygenase)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130910
[St] Status:MEDLINE


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[PMID]:22339770
[Au] Autor:Lee JH; Kim H; Woo JH; Joe EH; Jou I
[Ad] Endereço:Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon 442-721, Korea. if7979@hotmail.com
[Ti] Título:5, 8, 11, 14-eicosatetraynoic acid suppresses CCL2/MCP-1 expression in IFN-γ-stimulated astrocytes by increasing MAPK phosphatase-1 mRNA stability.
[So] Source:J Neuroinflammation;9:34, 2012 Feb 18.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The peroxisome proliferator-activated receptor (PPAR)-α activator, 5,8,11,14-eicosatetraynoic acid (ETYA), is an arachidonic acid analog. It is reported to inhibit up-regulation of pro-inflammatory genes; however, its underlying mechanism of action is largely unknown. In the present study, we focused on the inhibitory action of ETYA on the expression of the chemokine, CCL2/MCP-1, which plays a key role in the initiation and progression of inflammation. METHODS: To determine the effect of ETYA, primary cultured rat astrocytes and microglia were stimulated with IFN-γ in the presence of ETYA and then, expression of CCL2/MCP-1 and MAPK phosphatase (MKP-1) were determined using RT-PCR and ELISA. MKP-1 mRNA stability was evaluated by treating actinomycin D. The effect of MKP-1 and human antigen R (HuR) was analyzed by using specific siRNA transfection system. The localization of HuR was analyzed by immunocytochemistry and subcellular fractionation experiment. RESULTS: We found that ETYA suppressed CCL2/MCP-1 transcription and secretion of CCL2/MCP-1 protein through up-regulation of MKP-1mRNA levels, resulting in suppression of c-Jun N-terminal kinase (JNK) phosphorylation and activator protein 1 (AP1) activity in IFN-γ-stimulated brain glial cells. Moreover, these effects of ETYA were independent of PPAR-α. Experiments using actinomycin D revealed that the ETYA-induced increase in MKP-1 mRNA levels reflected an increase in transcript stability. Knockdown experiments using small interfering RNA demonstrated that this increase in MKP-1 mRNA stability depended on HuR, an RNA-binding protein known to promote enhanced mRNA stability. Furthermore, ETYA-induced, HuR-mediated mRNA stabilization resulted from HuR-MKP-1 nucleocytoplasmic translocation, which served to protect MKP-1 mRNA from the mRNA degradation machinery. CONCLUSION: ETYA induces MKP-1 through HuR at the post-transcriptional level in a receptor-independent manner. The mechanism revealed here suggests eicosanoids as potential therapeutic modulators of inflammation that act through a novel target.
[Mh] Termos MeSH primário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Astrócitos/efeitos dos fármacos
Quimiocina CCL2/metabolismo
Fosfatase 1 de Especificidade Dupla/genética
Interferon gama/farmacologia
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Córtex Cerebral/citologia
Imunoprecipitação da Cromatina
Proteínas ELAV
Ensaio de Desvio de Mobilidade Eletroforética
Inibidores Enzimáticos/farmacologia
Ensaio de Imunoadsorção Enzimática/métodos
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Microglia/efeitos dos fármacos
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Ratos
Ratos Sprague-Dawley
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (ELAV Proteins); 0 (Enzyme Inhibitors); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 82115-62-6 (Interferon-gamma); EC 3.1.3.48 (Dual Specificity Phosphatase 1)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120221
[St] Status:MEDLINE
[do] DOI:10.1186/1742-2094-9-34


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[PMID]:22203421
[Au] Autor:Cho YS; Kim CH; Kim KY; Cheon HG
[Ad] Endereço:Division of Drug Discovery, Korea Research Institute of Chemical Technology, P.O. Box 107, Yuseong-gu, Daejeon 305-600, Korea.
[Ti] Título:Protective effects of arachidonic acid against palmitic acid-mediated lipotoxicity in HIT-T15 cells.
[So] Source:Mol Cell Biochem;364(1-2):19-28, 2012 May.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Saturated fatty acids have been considered major contributing factors in type 2 diabetes, whereas unsaturated fatty acids have beneficial effects for preventing the development of diabetes. However, the effects of polyunsaturated fatty acids in pancreatic ß cells have not been reported. Here, we examined the effects of arachidonic acid (AA) on palmitic acid (PA)-mediated lipotoxicity in clonal HIT-T15 pancreatic ß cells. AA prevented the PA-induced lipotoxicity as indicated by cell viability, DNA fragmentation and mitochondrial membrane potential, whereas eicosatetraynoic acid (ETYA), a non-metabolizable AA, had little effect on PA-induced lipotoxicity. In parallel with its protective effects against PA-induced lipotoxicity, AA restored impaired insulin expression and secretion induced by PA. AA but not ETYA increased intracellular triglyceride (TG) in the presence of PA compared with PA alone, and xanthohumol, a diacylglycerol acyltransferase (DGAT) inhibitor, reversed AA-induced protection from PA. Taken together, our results suggest that AA protects against PA-induced lipotoxicity in clonal HIT-T15 pancreatic ß cells, and the protective effects may be associated with TG accumulation, possibly through sequestration of lipotoxic PA into TG.
[Mh] Termos MeSH primário: Ácido Araquidônico/metabolismo
Ácido Araquidônico/farmacologia
Ácido Palmítico/toxicidade
Substâncias Protetoras/farmacologia
Triglicerídeos/metabolismo
[Mh] Termos MeSH secundário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Animais
Sobrevivência Celular/efeitos dos fármacos
Cricetinae
Fragmentação do DNA/efeitos dos fármacos
Diabetes Mellitus Tipo 2/metabolismo
Diacilglicerol O-Aciltransferase/antagonistas & inibidores
Inibidores Enzimáticos/farmacologia
Ácidos Graxos/metabolismo
Ácidos Graxos Insaturados/metabolismo
Flavonoides/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Insulina/genética
Insulina/metabolismo
Células Secretoras de Insulina/metabolismo
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Propiofenonas/farmacologia
Substâncias Protetoras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Fatty Acids); 0 (Fatty Acids, Unsaturated); 0 (Flavonoids); 0 (Insulin); 0 (Propiophenones); 0 (Protective Agents); 0 (Triglycerides); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 27YG812J1I (Arachidonic Acid); 2V16EO95H1 (Palmitic Acid); EC 2.3.1.20 (Diacylglycerol O-Acyltransferase); T4467YT1NT (xanthohumol)
[Em] Mês de entrada:1209
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111229
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-011-1200-z


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[PMID]:21903824
[Au] Autor:Grald A; Yargosz P; Case S; Shea K; Johnson DI
[Ad] Endereço:Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT 05405, USA.
[Ti] Título:Small-molecule inhibitors of biofilm formation in laboratory and clinical isolates of Candida albicans.
[So] Source:J Med Microbiol;61(Pt 1):109-14, 2012 Jan.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Candida albicans cells have the ability to form biofilms on biotic and abiotic surfaces, such as indwelling medical devices. C. albicans cells can interconvert between budded and hyphal growth forms, herein termed the budded-to-hyphal transition (BHT), which is important for the formation of mature biofilms. Previous work identified 23 small organic molecules that could inhibit the BHT but did not affect C. albicans cell viability or budded cell growth. These BHT inhibitors were proposed to inhibit multiple signalling pathways regulating the BHT, many of which also regulate biofilm formation. However, only three of the BHT inhibitors, buhytrinA, ETYA and CGP-37157, were capable of inhibiting in vitro biofilm formation of wild-type laboratory C. albicans strains. When clinical C. albicans isolates were examined for their ability to form biofilms, only 11 of the 28 clinical isolates tested (39%) were capable of forming biofilms. Although buhytrinA, ETYA and CGP-37157 could inhibit the BHT of all 28 clinical isolates, they were only able to inhibit biofilm formation of a subset of these clinical isolates, with ETYA having 100% efficacy. These data indicate that the biofilm-forming capability of laboratory and clinical isolates of C. albicans, as well as the efficacy of BHT inhibitors against these different isolates, can differ dramatically. These differences between laboratory and clinical isolates should be an important aspect to consider when examining potentially new antifungal therapeutics.
[Mh] Termos MeSH primário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Antifúngicos/farmacologia
Biofilmes/efeitos dos fármacos
Candida albicans/efeitos dos fármacos
Clonazepam/análogos & derivados
Tiazepinas/farmacologia
[Mh] Termos MeSH secundário: Biofilmes/crescimento & desenvolvimento
Candida albicans/crescimento & desenvolvimento
Candida albicans/isolamento & purificação
Candida albicans/fisiologia
Candidíase/microbiologia
Clonazepam/farmacologia
Meios de Cultura
Seres Humanos
Hifas/efeitos dos fármacos
Hifas/fisiologia
Testes de Sensibilidade Microbiana
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Antifungal Agents); 0 (Culture Media); 0 (Thiazepines); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 5PE9FDE8GB (Clonazepam); 75450-34-9 (CGP 37157)
[Em] Mês de entrada:1202
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110910
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.034124-0


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[PMID]:21564022
[Au] Autor:Fang YJ; Zhou MH; Gao XF; Gu H; Mei YA
[Ad] Endereço:Institute of Brain Science, School of Life Sciences and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200433, China.
[Ti] Título:Arachidonic acid modulates Na+ currents by non-metabolic and metabolic pathways in rat cerebellar granule cells.
[So] Source:Biochem J;438(1):203-15, 2011 Aug 15.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AA (arachidonic acid), which possesses both neurotoxic and neurotrophic activities, has been implicated as a messenger in both physiological and pathophysiological processes. In the present study, we investigated the effects of both extracellular and intracellular application of AA on the activity of Na(V) (voltage-gated Na(+) channels) in rat cerebellar GCs (granule cells). The extracellular application of AA inhibited the resultant I(Na) (Na(V) current), wherein the current-voltage curve shifted to a negative voltage direction. Because this effect could be reproduced by treating the GCs with ETYA (eicosa-5,8,11,14-tetraynoic acid) or a membrane-impermeable analogue of AA, AA-CoA (arachidonoyl coenzyme A), we inferred that AA itself exerted the observed modulatory effects on I(Na). In contrast, intracellular AA significantly augmented the elicited I(Na) peak when the same protocol that was used for extracellular AA was followed. The observed I(Na) increase that was induced by intracellular AA was mimicked by the AA cyclo-oxygenase metabolite PGE(2) (prostaglandin E(2)), but not by ETYA. Furthermore, cyclo-oxygenase inhibitors decreased I(Na) and quenched AA-induced channel activation, indicating that the effect of intracellular AA on Na(V) was possibly mediated through AA metabolites. In addition, the PGE2-induced activation of I(Na) was mimicked by cAMP and quenched by a PKA (protein kinase A) inhibitor, a G(s) inhibitor and EP (E-series of prostaglandin) receptor antagonists. The results of the present study suggest that extracellular AA modulates Na(V) channel activity in rat cerebellar GCs without metabolic conversion, whereas intracellular AA augments the I(Na) by PGE(2)-mediated activation of cAMP/PKA pathways. These observations may explain the dual character of AA in neuronal pathogenesis.
[Mh] Termos MeSH primário: Ácido Araquidônico/farmacologia
Cerebelo/efeitos dos fármacos
Cerebelo/metabolismo
Potenciais da Membrana/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Canais de Sódio/metabolismo
Sódio/metabolismo
[Mh] Termos MeSH secundário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Animais
Encéfalo/citologia
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Células Cultivadas
Cerebelo/citologia
Ciclo-Oxigenase 2/química
Ciclo-Oxigenase 2/metabolismo
Inibidores de Ciclo-Oxigenase/farmacologia
Dinoprostona/metabolismo
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Técnicas de Patch-Clamp
RNA Mensageiro/genética
Ratos
Ratos Sprague-Dawley
Receptores de Prostaglandina E Subtipo EP1/genética
Receptores de Prostaglandina E Subtipo EP1/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cyclooxygenase Inhibitors); 0 (RNA, Messenger); 0 (Receptors, Prostaglandin E, EP1 Subtype); 0 (Sodium Channels); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 27YG812J1I (Arachidonic Acid); 9NEZ333N27 (Sodium); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1110
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110514
[St] Status:MEDLINE
[do] DOI:10.1042/BJ20110569


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[PMID]:21502285
[Au] Autor:Lee CJ; Gonçalves LL; Wells PG
[Ad] Endereço:Faculty of Pharmacy, University of Toronto, 144 College St., Toronto, ON, Canada.
[Ti] Título:Embryopathic effects of thalidomide and its hydrolysis products in rabbit embryo culture: evidence for a prostaglandin H synthase (PHS)-dependent, reactive oxygen species (ROS)-mediated mechanism.
[So] Source:FASEB J;25(7):2468-83, 2011 Jul.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thalidomide (TD) causes birth defects in humans and rabbits via several potential mechanisms, including bioactivation by embryonic prostaglandin H synthase (PHS) enzymes to a reactive intermediate that enhances reactive oxygen species (ROS) formation. We show herein that TD in rabbit embryo culture produces relevant embryopathies, including decreases in head/brain development by 28% and limb bud growth by 71% (P<0.05). Two TD hydrolysis products, 2-phthalimidoglutaramic acid (PGMA) and 2-phthalimidoglutaric acid (PGA), were similarly embryopathic, attenuating otic vesicle (ear) and limb bud formation by up to 36 and 77%, respectively (P<0.05). TD, PGMA, and PGA all increased embryonic DNA oxidation measured as 8-oxoguanine (8-oxoG) by up to 2-fold (P<0.05). Co- or pretreatment with the PHS inhibitors eicosatetraynoic acid (ETYA) or acetylsalicylic acid (ASA), or the free-radical spin trap phenylbutylnitrone (PBN), completely blocked embryonic 8-oxoG formation and/or embryopathies initiated by TD, PGMA, and PGA. This is the first demonstration of limb bud embryopathies initiated by TD, as well as its hydrolysis products, in a mammalian embryo culture model of a species susceptible to TD in vivo, indicating that all likely contribute to TD teratogenicity in vivo, in part through PHS-dependent, ROS-mediated mechanisms.
[Mh] Termos MeSH primário: Embrião de Mamíferos/efeitos dos fármacos
Teratogênios/toxicidade
Talidomida/toxicidade
[Mh] Termos MeSH secundário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Animais
Aspirina/farmacologia
Encéfalo/anormalidades
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Desoxiguanosina/análogos & derivados
Desoxiguanosina/metabolismo
Embrião de Mamíferos/anormalidades
Embrião de Mamíferos/metabolismo
Feminino
Hidrólise
Botões de Extremidades/anormalidades
Botões de Extremidades/efeitos dos fármacos
Botões de Extremidades/metabolismo
Masculino
Estrutura Molecular
Oxirredução/efeitos dos fármacos
Prostaglandina-Endoperóxido Sintases/metabolismo
Coelhos
Espécies Reativas de Oxigênio/metabolismo
Teratogênios/química
Teratogênios/metabolismo
Talidomida/química
Talidomida/metabolismo
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (Teratogens); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 4Z8R6ORS6L (Thalidomide); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases); G9481N71RO (Deoxyguanosine); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1109
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110420
[St] Status:MEDLINE
[do] DOI:10.1096/fj.10-178814


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[PMID]:19729221
[Au] Autor:Taheri P; Tarighi S
[Ad] Endereço:Department of Crop Protection, Faculty of Agriculture, Ferdowsi University of Mashhad, P.O. Box 91775-1163, Mashhad, Iran. Marta
[Ti] Título:Riboflavin induces resistance in rice against Rhizoctonia solani via jasmonate-mediated priming of phenylpropanoid pathway.
[So] Source:J Plant Physiol;167(3):201-8, 2010 Feb 15.
[Is] ISSN:1618-1328
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Vitamins are plant growth regulators and activators of defense responses against pathogens. The cytomolecular mechanisms involved in the induction of resistance by chemicals especially vitamins on monocotyledonous plants are largely unknown. Here, we show that riboflavin, which acts as a defense activator in rice against economically important sheath blight caused by Rhizoctonia solani, primed the expression of lipoxygenase (LOX) as a key gene in octadecanoid pathway, and enhanced lignification. Exogenous jasmonic acid (JA) application on rice induces resistance against R. solani in a manner similar to riboflavin. Application of jasmonate-deficient rice mutant hebiba and using a LOX inhibitor revealed the main role of octadecanoid pathway in riboflavin-induced resistance (IR). In riboflavin-treated inoculated plants, upregulation of phenylalanine ammonia-lyase (PAL) expression, as a major marker of phenylpropanoid pathway, was detected downstream of LOX upregulation. Co-application of riboflavin and 5, 8, 11, 14-eicosatetraynoic acid (ETYA) on rice leaves revealed no upregulation of PAL and no priming in lignification. Furthermore, lower levels of PAL transcripts and lignin were detected in hebiba compared with control. These findings indicate the role of octadecanoid pathway in the induction of phenylpropanoid metabolism leading to lignification as a novel mechanism of riboflavin-IR in Oryza sativa-R. solani pathosystem.
[Mh] Termos MeSH primário: Peróxido de Hidrogênio/metabolismo
Lignina/metabolismo
Oryza/imunologia
Rhizoctonia/fisiologia
Riboflavina/farmacologia
[Mh] Termos MeSH secundário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Ciclopentanos/farmacologia
Interações Hospedeiro-Patógeno
Lipoxigenase/metabolismo
Inibidores de Lipoxigenase/farmacologia
Oryza/metabolismo
Oryza/microbiologia
Oxilipinas/farmacologia
Fenilalanina Amônia-Liase/metabolismo
Doenças das Plantas/imunologia
Folhas de Planta/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cyclopentanes); 0 (Lipoxygenase Inhibitors); 0 (Oxylipins); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 6RI5N05OWW (jasmonic acid); 9005-53-2 (Lignin); BBX060AN9V (Hydrogen Peroxide); EC 1.13.11.12 (Lipoxygenase); EC 4.3.1.24 (Phenylalanine Ammonia-Lyase); TLM2976OFR (Riboflavin)
[Em] Mês de entrada:1004
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090905
[St] Status:MEDLINE
[do] DOI:10.1016/j.jplph.2009.08.003


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[PMID]:19487023
[Au] Autor:Ratz PH; Miner AS; Barbour SE
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Virginia Commonwealth University School of Medicine, USA. phratz@vcu.edu
[Ti] Título:Calcium-independent phospholipase A2 participates in KCl-induced calcium sensitization of vascular smooth muscle.
[So] Source:Cell Calcium;46(1):65-72, 2009 Jul.
[Is] ISSN:1532-1991
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In vascular smooth muscle, KCl not only elevates intracellular free Ca(2+) ([Ca(2+)](i)), myosin light chain kinase activity and tension (T), but also can inhibit myosin light chain phosphatase activity by activation of rhoA kinase (ROCK), resulting in Ca(2+) sensitization (increased T/[Ca(2+)](i) ratio). Precisely how KCl causes ROCK-dependent Ca(2+) sensitization remains to be determined. Using Fura-2-loaded isometric rings of rabbit artery, we found that the Ca(2+)-independent phospholipase A(2) (iPLA(2)) inhibitor, bromoenol lactone (BEL), reduced the KCl-induced tonic but not early phasic phase of T and potentiated [Ca(2+)](i), reducing Ca(2+) sensitization. The PKC inhibitor, GF-109203X (> or =3 microM) and the pseudo-substrate inhibitor of PKCzeta produced a response similar to BEL. BEL reduced basal and KCl-stimulated myosin phosphatase phosphorylation. Whereas BEL and H-1152 produced strong inhibition of KCl-induced tonic T (approximately 50%), H-1152 did not induce additional inhibition of tissues already inhibited by BEL, suggesting that iPLA(2) links KCl stimulation with ROCK activation. The cPLA(2) inhibitor, pyrrolidine-1, inhibited KCl-induced tonic increases in [Ca(2+)](i) but not T, whereas the inhibitor of 20-HETE production, HET0016, acted like the ROCK inhibitor H-1152 by causing Ca(2+) desensitization. These data support a model in which iPLA(2) activity regulates Ca(2+) sensitivity.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Músculo Liso Vascular/enzimologia
Fosfolipases A2 Independentes de Cálcio/metabolismo
Cloreto de Potássio/farmacologia
[Mh] Termos MeSH secundário: Ácido 5,8,11,14-Eicosatetrainoico/farmacologia
Animais
Ácido Araquidônico/antagonistas & inibidores
Cinética
Contração Muscular/efeitos dos fármacos
Tono Muscular/efeitos dos fármacos
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Quinase de Cadeia Leve de Miosina/metabolismo
Naftalenos/farmacologia
Fenilefrina/farmacologia
Proteína Quinase C/antagonistas & inibidores
Pironas/farmacologia
Pirrolidinas/farmacologia
Coelhos
Quinases Associadas a rho/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Naphthalenes); 0 (Pyrones); 0 (Pyrrolidines); 1191-85-1 (5,8,11,14-Eicosatetraynoic Acid); 1WS297W6MV (Phenylephrine); 27YG812J1I (Arachidonic Acid); 660YQ98I10 (Potassium Chloride); 88070-98-8 (6-(bromomethylene)tetrahydro-3-(1-naphthaleneyl)-2H-pyran-2-one); EC 2.7.11.1 (protein kinase C zeta); EC 2.7.11.1 (rho-Associated Kinases); EC 2.7.11.13 (Protein Kinase C); EC 2.7.11.18 (Myosin-Light-Chain Kinase); EC 3.1.1.4 (Phospholipases A2, Calcium-Independent); LJU5627FYV (pyrrolidine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0908
[Cu] Atualização por classe:161122
[Lr] Data última revisão:
161122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090603
[St] Status:MEDLINE
[do] DOI:10.1016/j.ceca.2009.05.001



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