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[PMID]:29217480
[Au] Autor:Aichinger G; Puntscher H; Beisl J; Kütt ML; Warth B; Marko D
[Ad] Endereço:Department of Food Chemistry and Toxicology, Faculty of Chemistry, University of Vienna, Waehringerstr. 38, A-1090 Vienna, Austria.
[Ti] Título:Delphinidin protects colon carcinoma cells against the genotoxic effects of the mycotoxin altertoxin II.
[So] Source:Toxicol Lett;284:136-142, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Alternaria spp. are ubiquitous molds that are able to produce toxic secondary metabolites which may contaminate food globally. One of those is the mycotoxin altertoxin II (ATX-II), a genotoxic and mutagenic compound. In recent years, different flavonoids that may co-occur with mycotoxins in food were demonstrated to temper toxic effects of molds, mostly through their anti-oxidant properties. Thus, in this study, we assessed the influence of the berry anthocyanidin delphinidin on the toxicity of ATX-II in HT-29 colon carcinoma cells. We performed coupled SRB/WST-1 cytotoxicity assays which revealed only weak antagonistic interactions, and single-cell gel electrophoresis ("comet") assays, where we observed a potent protective effect of delphinidin on the DNA-damaging properties of ATX-II. Furthermore, we investigated the mechanism for this interaction. In the DCF assay delphinidin was found to reduce intracellular oxidative stress levels, which might contribute partly to the latter protection. However, LC-MS experiments showed that co-incubation of the mycotoxin with either delphinidin or its potential degradation product phloroglucinol aldehyde significantly decreased ATX-II concentrations in aqueous solutions, indicating that a direct chemical reaction of ATX-II with these components is likely responsible for the observed loss of toxicity. Our results indicate that delphinidin - and possibly other anthocyanins as well - might play a role in the protection of the gut from Alternaria-induced genotoxicity.
[Mh] Termos MeSH primário: Antocianinas/farmacologia
Antioxidantes/farmacologia
Benzo(a)Antracenos/toxicidade
Dano ao DNA/efeitos dos fármacos
Mutagênicos/toxicidade
[Mh] Termos MeSH secundário: Alternaria/crescimento & desenvolvimento
Alternaria/metabolismo
Benzo(a)Antracenos/isolamento & purificação
Contagem de Células
Técnicas de Cultura de Células
Sobrevivência Celular/efeitos dos fármacos
Ensaio Cometa
Relação Dose-Resposta a Droga
Microbiologia de Alimentos
Células HT29
Seres Humanos
Estrutura Molecular
Mutagênicos/isolamento & purificação
Estresse Oxidativo/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Antioxidants); 0 (Benz(a)Anthracenes); 0 (Mutagens); 56257-59-1 (altertoxin II); EM6MD4AEHE (delphinidin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


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[PMID]:28922594
[Au] Autor:Pink M; Verma N; Zerries A; Schmitz-Spanke S
[Ad] Endereço:Institute and Outpatient Clinic of Occupational, Social and Environmental Medicine, University of Erlangen-Nuremberg , Schillerstr. 25/29, 91054 Erlangen, Germany.
[Ti] Título:Dose-Dependent Response to 3-Nitrobenzanthrone Exposure in Human Urothelial Cancer Cells.
[So] Source:Chem Res Toxicol;30(10):1855-1864, 2017 Oct 16.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A product of incomplete combustion of diesel fuel, 3-nitrobenzanthrone (3-NBA), has been classified as a cancer-causing substance. It first gained attention as a potential urinary bladder carcinogen due to the presence of its metabolite in urine and formation of DNA adducts. The aim of the present study was to characterize the dose-response relationship of 3-NBA in human urothelial cancer cell line (RT4) exposed to concentrations ranging from 0.0003 µM (environmentally relevant) to 80 µM by utilizing toxicological and metabolomic approaches. We observed that the RT4 cells were capable of bioactivation of 3-NBA within 30 min of exposure. Activity measurements of various enzymes involved in the conversion of 3-NBA in RT4 cells demonstrated NAD(P)H:quinone oxidoreductase (NQO1) as the main contributor for its bioactivation. Moreover, cytotoxicity assessment exhibited an initiation of adaptive mechanisms at low dosages, which diminished at higher doses, indicating that the capacity of these mechanisms no longer suffices, resulting in increased levels of intracellular reactive oxygen species, reduced proliferation, and hyperpolarisation of the mitochondrial membrane. To characterize the underlying mechanisms of this cellular response, the metabolism of 3-NBA and metabolomic changes in the cells were analyzed. The metabolomic analysis of the cells (0.0003, 0.01, 0.08, 10, and 80 µM 3-NBA) showed elevated levels of various antioxidants at low concentrations of 3-NBA. However, at higher exposure concentrations, it appeared that the cells reprogrammed their metabolism to maintain the cell homeostasis via activation of pentose phosphate pathway (PPP).
[Mh] Termos MeSH primário: Benzo(a)Antracenos/administração & dosagem
Benzo(a)Antracenos/farmacologia
Neoplasias da Bexiga Urinária/induzido quimicamente
[Mh] Termos MeSH secundário: Benzo(a)Antracenos/química
Benzo(a)Antracenos/toxicidade
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Estrutura Molecular
Via de Pentose Fosfato/efeitos dos fármacos
Relação Estrutura-Atividade
Neoplasias da Bexiga Urinária/metabolismo
Neoplasias da Bexiga Urinária/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-nitrobenzanthrone); 0 (Benz(a)Anthracenes)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.7b00174


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[PMID]:28628210
[Au] Autor:Chatterjee A; Malik CK; Basu AK
[Ad] Endereço:Department of Chemistry, University of Connecticut, Storrs, Connecticut.
[Ti] Título:Synthesis of Oligodeoxynucleotides Containing a C8-2'-Deoxyguanosine Adduct Formed by the Carcinogen 3-Nitrobenzanthrone.
[So] Source:Curr Protoc Nucleic Acid Chem;69:4.73.1-4.73.15, 2017 Jun 19.
[Is] ISSN:1934-9289
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This unit describes the detailed procedure in five parts for the synthesis of the C8-2'-deoxyguanosine-3-aminobenzanthrone adduct located in a desired site in an oligonucleotide. The synthesis of the protected 2'-deoxyguanosine, O -benzyl-N -DMTr-3'-5'-bisTBDMS-C8-Br-2'-deoxyguanosine, is described in the first part. The synthesis of the reduced carcinogen 3-aminobenzanthrone is detailed in part two. The third part outlines the key step of the adduct formation between the reduced carcinogen and the protected nucleoside by a palladium-catalyzed cross coupling reaction. The final two parts describe phosphoramidite synthesis from the nucleoside-carcinogen adduct followed by its site-specific incorporation into DNA by solid-phase oligonucleotide synthesis. The adducted oligonucleotides are purified by reversed-phase HPLC and characterized by mass spectrometry. © 2017 by John Wiley & Sons, Inc.
[Mh] Termos MeSH primário: Benzo(a)Antracenos/química
Carcinógenos/química
Desoxiguanosina/química
Oligodesoxirribonucleotídeos/síntese química
[Mh] Termos MeSH secundário: Automação
Espectroscopia de Ressonância Magnética Nuclear de Carbono-13
Oligodesoxirribonucleotídeos/química
Espectroscopia de Prótons por Ressonância Magnética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-nitrobenzanthrone); 0 (Benz(a)Anthracenes); 0 (Carcinogens); 0 (Oligodeoxyribonucleotides); G9481N71RO (Deoxyguanosine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1002/cpnc.28


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[PMID]:28495615
[Au] Autor:Tewari P; Mandal P; Roy R; Asthana S; Dwivedi PD; Das M; Tripathi A
[Ad] Endereço:Food Toxicology Lab, Food, Drug and Chemical Toxicology Group, CSIR- Indian Institute of Toxicology Research, Vishvigyan Bhawan 31,Mahatma Gandhi Marg, Lucknow, 226001, Uttar Pradesh, India; Academy of Scientific & Innovative Research (AcSIR), CSIR-IITR Campus, Lucknow, India.
[Ti] Título:A novel function of TLR4 in mediating the immunomodulatory effect of Benzanthrone, an environmental pollutant.
[So] Source:Toxicol Lett;276:69-84, 2017 Jul 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Our prior studies have reported that Benzanthrone (BA) manifests inflammatory responses in the spleen of Balb/c mice. The present investigation was carried out to study the impact of BA on macrophages, which are the primary scavenger cells in the body that act as a connecting link between innate and adaptive immunity. Parenteral administration of BA (daily for one week) to mice resulted in enhanced levels of nitric oxide (NO) and overexpression of inflammatory markers (COX-2, MMP-9 and PGE-2) in macrophages; however the level of MHC class-I and MHC class-II receptors were down regulated. Further, the potential membrane receptor targets (TLRs) of BA and its interaction with TLRs was investigated using computational methods. Professional phagocytes play pivotal roles in sensing bacteria through pathogen-associated molecular patterns (PAMPs) by various pathogen recognition receptors (PRRs), including Toll-like receptors (TLRs). Several studies have implicated these TLRs in the amplification of the inflammatory responses, however the fundamental role played by TLRs in mediating the inflammation associated with xenobiotics is still obscure and not understood. From the in silico analysis, it was evident that BA showed the highest binding affinity with TLR4 as compared to other TLRs. The western blotting studies confirmed that BA exposure indeed upregulated the expression of TLR 4, 5 and 9. Moreover, the downstream signaling cascade proteins of TLRs such as myeloid differentiation primary response protein-88 (MyD88), IL-1 receptor associated kinase (IRAK-1), and TNFR-associated factor (TRAF-6) were found to be enhanced in the BA treated groups. It was also observed that BA treatment increased the expression of ICAM-1, p-Lyn, p-Syk, p-PI3-K, IP , PLC-γ, cAMP and Ca influx, which are known to play a critical role in TLR mediated inflammation. Earlier we found that toxic effects of BA in spleen were mediated by oxidative stress which was partially neutralized by NAC exposure. Hereby, we report that NAC treatment in conjunction with BA attenuated the expression of BA induced TLR4, as well as the inflammatory markers such as COX2 and p-NFkB in macrophages. These findings demonstrated the critical role of TLRs in the regulation of the BA-induced inflammation.
[Mh] Termos MeSH primário: Benzo(a)Antracenos/toxicidade
Poluentes Ambientais/toxicidade
Inflamação/induzido quimicamente
Macrófagos Peritoneais/efeitos dos fármacos
Receptor 4 Toll-Like/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/farmacologia
Antioxidantes/farmacologia
Benzo(a)Antracenos/metabolismo
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Relação Dose-Resposta a Droga
Poluentes Ambientais/metabolismo
Feminino
Inflamação/genética
Inflamação/imunologia
Inflamação/metabolismo
Mediadores da Inflamação/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Macrófagos Peritoneais/imunologia
Macrófagos Peritoneais/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Simulação de Acoplamento Molecular
Estresse Oxidativo/efeitos dos fármacos
Fagocitose/efeitos dos fármacos
Ligação Proteica
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/genética
Receptor 4 Toll-Like/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Benz(a)Anthracenes); 0 (Environmental Pollutants); 0 (Icam1 protein, mouse); 0 (Inflammation Mediators); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 1.14.99.- (Ptgs2 protein, mouse); EC 1.14.99.1 (Cyclooxygenase 2); LP5P3RR8QN (benzanthrone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE


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[PMID]:28382548
[Au] Autor:Terzopoulou E; Voutsa D
[Ad] Endereço:Laboratory of Environmental Pollution Control, Department of Chemistry, Aristotle University, Thessaloniki, 54124, Greece.
[Ti] Título:Study of persistent toxic pollutants in a river basin-ecotoxicological risk assessment.
[So] Source:Ecotoxicology;26(5):625-638, 2017 Jul.
[Is] ISSN:1573-3017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study presents a complementary approach for the evaluation of water quality in a river basin by employing active and passive sampling. Persistent toxic pollutants representing three classes: organochlorinated pesticides (OCPs), polychlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAHs), were studied in grab water samples, in passive samplers/SemiPermeable Membrane Devices (SPMDs) and in fish tissues collected along the Strymonas River, northern Greece at three sampling campaigns during the year 2013. Almost all the target compounds were detected in the study river of Strymonas, northern Greece at the periods of high rainfall intensity and/or low flow-rate. The most frequently detected compounds were 1,2-benzanthracene, benzo(a)pyrene, benzo(b)fluoranthene, endosulfan I, endosulfan II, endosulfan sulfate, endrin aldehyde, fluorene, methoxychlor, polychlorinated biphenyl PCB 28, PCB 180 and pyrene. The family of DDT compounds and aldrin were also occasionally detected. Agricultural run-off and waste effluents are the main sources of hydrophobic organic compounds in the river basin. The use of SPMDs allowed the detection of more micropollutants than active sampling (31 vs. 16, respectively). Results showed relatively low risk however the potential risk associated with micropollutants such as 1,2-benzanthracene, benzo(b)fluoranthene, p,p-dichlorodiphenyldichloroethane (DDD), endosulfan II, methoxychlor, PCB 180 and pyrene should not be neglected. Performing risk assessment based on passive sampling, more information was obtained about temporal and spatial variation. SPMDs could be applied as a pre-evaluation before chemical monitoring in biota.
[Mh] Termos MeSH primário: Monitoramento Ambiental
Poluentes Químicos da Água/análise
[Mh] Termos MeSH secundário: Benzo(a)Antracenos/análise
Ecotoxicologia
Endossulfano/análogos & derivados
Fluorenos/análise
Grécia
Hidrocarbonetos Clorados/análise
Compostos Orgânicos/análise
Praguicidas/análise
Bifenilos Policlorados/análise
Hidrocarbonetos Aromáticos Policíclicos/análise
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benz(a)Anthracenes); 0 (Fluorenes); 0 (Hydrocarbons, Chlorinated); 0 (Organic Chemicals); 0 (Pesticides); 0 (Polycyclic Aromatic Hydrocarbons); 0 (Water Pollutants, Chemical); 3Q2UY0968A (fluorene); 52I0CG8IQX (PCB 180); 844ODP31Q0 (2,4,4'-trichlorobiphenyl); 8QTV9M19B2 (endosulfan sulfate); C5PLF6152K (benz(a)anthracene); DFC2HB4I0K (Polychlorinated Biphenyls); OKA6A6ZD4K (Endosulfan)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1007/s10646-017-1795-2


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[PMID]:28096451
[Au] Autor:White PA; Douglas GR; Phillips DH; Arlt VM
[Ad] Endereço:Environmental Health Science and Research Bureau, Health Canada, Tunney's Pasture 0803A, 50 Colombine Driveway, Ottawa, Ontario K1A 0K9, Canada and.
[Ti] Título:Quantitative relationships between lacZ mutant frequency and DNA adduct frequency in Muta™Mouse tissues and cultured cells exposed to 3-nitrobenzanthrone.
[So] Source:Mutagenesis;32(2):299-312, 2017 Mar 01.
[Is] ISSN:1464-3804
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The frequency of stable DNA adducts in a target tissue can be used to assess biologically effective dose; however, the utility of the metric in a risk assessment context depends on the likelihood that the DNA damage will be manifested as mutation. Previously, we employed the Muta™Mouse system to examine the induction of lacZ mutants and DNA adducts following exposure to the well-studied mutagenic carcinogen 3-nitrobenzanthrone (3-NBA). In this follow-up work, we examined the empirical relationships between total adduct frequency and mutant frequency (MF) in tissues and cultured cells following acute 3-NBA exposure. The results show a significant induction of DNA damage and lacZ mutants in liver, colon and bone marrow, as well as FE1 pulmonary epithelial cells. In contrast, lung and small intestine samples had low, but significantly elevated adduct levels, with no significant increases in lacZ MF. Additional analyses showed a significant relationship between the mutagenic efficiency of total adducts, measured as the slope of the relationships between MF and total adduct frequency, and tissue-specific mitotic index (MI). The lack of mutation response in lung, in contrast to the high in vitro MF in FE-1 lung cells, is likely related to the 100-fold difference in MI. The lack of small intestine mutagenic response may be related to limited metabolic capacity, differences in DNA repair, and /or chemically induced apoptosis that has been observed for other potent mutagens. The results indicate that interpretation of adduct frequency values in a risk assessment context can be improved by considering the MI of the target tissue; however, more generalised interpretation is hampered by tissue-specific variations in metabolic capacity and damage processing. The work provides a proof of principle regarding the use of the Muta™Mouse system to critically examine the health risks associated with tissue-specific adduct loads.
[Mh] Termos MeSH primário: Benzo(a)Antracenos/toxicidade
Adutos de DNA/metabolismo
Reparo do DNA
Óperon Lac/efeitos dos fármacos
Mutação
[Mh] Termos MeSH secundário: Animais
Adutos de DNA/análise
Dano ao DNA
Óperon Lac/genética
Masculino
Camundongos
Testes de Mutagenicidade
Especificidade de Órgãos
Transgenes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-nitrobenzanthrone); 0 (Benz(a)Anthracenes); 0 (DNA Adducts)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1093/mutage/gew067


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[PMID]:28029781
[Au] Autor:Abbas S; Alam S; Singh KP; Kumar M; Gupta SK; Ansari KM
[Ad] Endereço:Department of Biochemistry, School of Dental Sciences, Babu Banarsi Das University (BBDU) , Faizabad Road, Lucknow, Uttar Pradesh 226028, India.
[Ti] Título:Aryl Hydrocarbon Receptor Activation Contributes to Benzanthrone-Induced Hyperpigmentation via Modulation of Melanogenic Signaling Pathways.
[So] Source:Chem Res Toxicol;30(2):625-634, 2017 Feb 20.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Benzanthrone (BA), an oxidized polycyclic aromatic hydrocarbon (PAH), has been found to be a potential health threat to occupational workers involved in dye manufacturing factories. It has been observed that occupational workers become exposed to BA either during manufacturing, pulverization, or storage and developed various kinds of skin diseases like contact dermatitis, itching, erythema, roughness, and foremost, hyperpigmentation. It has been shown that some environmental organic pollutants (POPs) like dioxins, furans, and polychlorinated biphenyls (PCBs) may act as ligands for the aryl hydrocarbon receptor (AhR) and regulate hyperpigmentation. Here, we hypothesized that BA may also act as a ligand for AhR and possibly regulate the melanogenic pathway to induced hyperpigmentation. Our computation results indicate that BA has a high binding affinity toward AhR for the initiation of melanogenic signaling. Following the in silico predictions, we used primary mouse melanocytes (PMMs) and confirmed that exposure to BA (5, 10, and 25 µM) resulted in an increase in AhR expression, tyrosinase activity, and melanin synthesis. Moreover, to study the physiological relevance of these findings, C57BL/6 mice were topically exposed to BA, and enhanced pigmentation and melanin synthesis were observed. Furthermore, the study was extended to assess the mechanistic aspects involved in BA-induced hyperpigmentation in PMMs as well as in mouse skin. Our results suggest that BA exposure initiates AhR signaling and increases tyrosinase enzyme activity and melanin synthesis. Moreover, the genes that regulate the melanin synthesis, such as TRP-1, TRP-2 and the transcription factor MITF, were also found to be increased. Thus, altogether, we suggest that BA-AhR interactions are critical for BA-induced hyperpigmentation.
[Mh] Termos MeSH primário: Benzo(a)Antracenos/toxicidade
Melaninas/metabolismo
Transtornos da Pigmentação/induzido quimicamente
Receptores de Hidrocarboneto Arílico/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Camundongos
Camundongos Endogâmicos C57BL
Simulação de Acoplamento Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benz(a)Anthracenes); 0 (Melanins); 0 (Receptors, Aryl Hydrocarbon); LP5P3RR8QN (benzanthrone)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161229
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.6b00364


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[PMID]:28007639
[Au] Autor:Vejdovszky K; Sack M; Jarolim K; Aichinger G; Somoza MM; Marko D
[Ad] Endereço:University of Vienna, Faculty of Chemistry, Department of Food Chemistry and Toxicology, Waehringer Str. 38, A-1090 Vienna, Austria.
[Ti] Título:In vitro combinatory effects of the Alternaria mycotoxins alternariol and altertoxin II and potentially involved miRNAs.
[So] Source:Toxicol Lett;267:45-52, 2017 Feb 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Alternariol (AOH) and altertoxin II (ATX II) are mycotoxins formed by Alternaria spp. Since they are expected to co-occur in Alternaria-infested food and feed, we addressed the question of combinatory effects. In addition, potentially involved regulatory microRNAs were surveyed in an exploratory approach. Cytotoxicity measurements in constant ratio combinations of 1:10 or 1:1 (ATX II: AOH) mainly revealed additive effects in HepG2, HT29 and HCEC-1CT cells. Yet, in specific high doses antagonism was found. Microarray analysis of miRNA expression profiles in HepG2 cells indicated different patterns of miRNA regulation by AOH and ATX II, including several miRNA species for which no distinct functions are currently known. Among others, miR-4654, miR-4715_3p and miR-6720_3p were up-regulated by AOH and miR-5583_5p was down-regulated by ATX II. Additionally, miR-1323, involved in hindering DNA repair mechanisms, was decreased by ATX II. Digital droplet PCR (ddPCR) analysis of selected miRNAs indicated regulation of miR-29a by AOH, which might play a role in AOH-induced apoptosis. miR-192 and miR-224 regulation was associated with antagonistic cytotoxic effects of AOH and ATX II combinations. Our study represents the first evaluation on combinatory effects of AOH and ATX II.
[Mh] Termos MeSH primário: Alternaria/metabolismo
Benzo(a)Antracenos/toxicidade
Contaminação de Alimentos
Lactonas/toxicidade
MicroRNAs/genética
[Mh] Termos MeSH secundário: Relação Dose-Resposta a Droga
Perfilação da Expressão Gênica/métodos
Regulação da Expressão Gênica
Células HT29
Células Hep G2
Seres Humanos
MicroRNAs/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benz(a)Anthracenes); 0 (Lactones); 0 (MIRN192 microRNA, human); 0 (MIRN224 microRNA, human); 0 (MicroRNAs); 56257-59-1 (altertoxin II); KN9L4260JW (alternariol)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE


  9 / 3330 MEDLINE  
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[PMID]:27843017
[Au] Autor:Yakan SD; Focks A; Klasmeier J; Okay OS
[Ad] Endereço:Istanbul Technical University, Faculty of Naval Architecture and Ocean Engineering, 34469, Maslak, Istanbul, Turkey. Electronic address: yakans@itu.edu.tr.
[Ti] Título:Numerical evaluation of bioaccumulation and depuration kinetics of PAHs in Mytilus galloprovincialis.
[So] Source:Environ Pollut;220(Pt B):1244-1250, 2017 Jan.
[Is] ISSN:1873-6424
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Polycyclic aromatic hydrocarbons (PAHs) are important organic pollutants in the aquatic environment due to their persistence and bioaccumulation potential both in organisms and in sediments. Benzo(a)anthracene (BaA) and phenanthrene (PHE), which are in the priority pollutant list of the U.S. EPA (Environmental Protection Agency), are selected as model compounds of the present study. Bioaccumulation and depuration experiments with local Mediterranean mussel species, Mytilus galloprovincialis were used as the basis of the study. Mussels were selected as bioindicator organisms due to their broad geographic distribution, immobility and low enzyme activity. Bioaccumulation and depuration kinetics of selected PAHs in Mytilus galloprovincialis were described using first order kinetic equations in a three compartment model. The compartments were defined as: (1) biota (mussel), (2) surrounding environment (seawater), and (3) algae (Phaeodactylum tricornutum) as food source of the mussels. Experimental study had been performed for three different concentrations. Middle concentration of the experimental data was used as the model input in order to represent other high and low concentrations of selected PAHs. Correlations of the experiment and model data revealed that they are in good agreement. Accumulation and depuration trend of PAHs in mussels regarding also the durations can be estimated effectively with the present study. Thus, this study can be evaluated as a supportive tool for risk assessment in addition to monitoring studies.
[Mh] Termos MeSH primário: Benzo(a)Antracenos/farmacocinética
Diatomáceas/metabolismo
Mytilus/metabolismo
Fenantrenos/farmacocinética
Poluentes Químicos da Água/farmacocinética
[Mh] Termos MeSH secundário: Animais
Cinética
Água do Mar/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benz(a)Anthracenes); 0 (Phenanthrenes); 0 (Water Pollutants, Chemical); 448J8E5BST (phenanthrene); C5PLF6152K (benz(a)anthracene)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE


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[PMID]:27840401
[Au] Autor:Lee HW; Kim YJ; Nam SJ; Kim H
[Ad] Endereço:Department of Pharmacy and Research Institute of Life Pharmaceutical Sciences, Sunchon National University, Suncheon 57922, Republic of Korea.
[Ti] Título:Potent Selective Inhibition of Monoamine Oxidase A by Alternariol Monomethyl Ether Isolated from .
[So] Source:J Microbiol Biotechnol;27(2):316-320, 2017 Feb 28.
[Is] ISSN:1738-8872
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Alternariol monomethyl ether (AME), a dibenzopyrone derivative, was isolated from along with altertoxin II (ATX-II). The compounds were tested for the inhibitory activity of monoamine oxidase (MAO), which catalyzes neurotransmitting monoamines. AME was found to be a highly potent and selective inhibitor of human MAO-A with an IC value of 1.71 µM; however, it was found to be ineffective for MAO-B inhibition. ATX-II was not effective for the inhibition of either MAO-A or MAO-B. The inhibition of MAO-A using AME was apparently instantaneous. MAO-A activity was almost completely recovered after the dilution of the inhibited enzyme with an excess amount of AME, suggesting AME is a reversible inhibitor. AME showed mixed inhibition for MAO-A in Lineweaver-Burk plots with a value of 0.34 µM. The findings of this study suggest that microbial metabolites and dibenzopyrone could be potent MAO inhibitors. In addition, AME could be a useful lead compound for developing reversible MAO-A inhibitors to treat depression, Parkinson's disease, and Alzheimer's disease.
[Mh] Termos MeSH primário: Alternaria/química
Lactonas/farmacologia
Inibidores da Monoaminoxidase/farmacologia
Monoaminoxidase/metabolismo
[Mh] Termos MeSH secundário: Alternaria/enzimologia
Doença de Alzheimer/tratamento farmacológico
Benzo(a)Antracenos/química
Benzo(a)Antracenos/isolamento & purificação
Depressão/tratamento farmacológico
Seres Humanos
Concentração Inibidora 50
Cinética
Lactonas/isolamento & purificação
Doença de Parkinson/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benz(a)Anthracenes); 0 (Lactones); 0 (Monoamine Oxidase Inhibitors); 56257-59-1 (altertoxin II); EC 1.4.3.4 (Monoamine Oxidase); EC 1.4.3.4. (monoamine oxidase A, human); Y79STA800H (alternariol monomethyl ether)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE
[do] DOI:10.4014/jmb.1610.10053



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