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Pesquisa : D27.888.569.100.125 [Categoria DeCS]
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[PMID]:29446294
[Au] Autor:Efimova NV; Rukavishnikov VS; Pankov VA; Perezhogin AN; Shayakhmetov SF; Meshchakova NM; Lisetskaya LG
[Ti] Título:[Assessment of carcinogenic risks to workers of the main enterprises of the Irkutsk region].
[So] Source:Gig Sanit;95(12):1163-7, 2016.
[Is] ISSN:0016-9900
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The purpose of research is the assessment of the individual cancer risk (ICR) for workers of the basic occupations in key branches of industry of the Irkutsk region. There was executed the calculation of ICR levels for workers of the basic occupations of the aircraft industry, aluminum smelters and vinyl chloride production plants. The estimation of the exposure for workers was carried out according to long-term time-weighted average concentrations in the air of the working area, for the population - on annual average concentrations in the ambient air. To assess the risk that is not associated with the profession, the dose was calculated for the period of life (70 years). When calculating the toxicant doses in the working area there were used the "standard" indices ofpulmonary ventilation for adults, body weight, the work experience in the contact with carcinogens of 30 years, the number of days in the contact of 240, the duration of the working time 8 or 12 hours (in accordance with the working hours) duration. ICR for the Irkutsk population amounted of 3.08E-04, in Shelekhov - 4.8E-05, Sayansk - 1.1E-05. The amount of risk depends on the content offormaldehyde in all territories and chromium VI in cities of Irkutsk and Shelekhov. ICR for workers of basic occupations of studied plants in dozens of times are higher than for the urban population. Priority carcinogens are: chromium VI, nickel, formaldehyde, silicon dioxide -for the aircraft plant employees; 1,2-dichloretan, vinyl chloride - for the workers of vinyl chloride production plant; benzopyrene - for the aluminum smelter workers.
[Mh] Termos MeSH primário: Poluentes Ocupacionais do Ar
Carcinogênese/induzido quimicamente
Cromo
Formaldeído
Indústria Manufatureira
Cloreto de Vinil
[Mh] Termos MeSH secundário: Poluentes Ocupacionais do Ar/análise
Poluentes Ocupacionais do Ar/toxicidade
Carcinógenos Ambientais/análise
Carcinógenos Ambientais/toxicidade
Cromo/análise
Cromo/toxicidade
Formaldeído/análise
Formaldeído/toxicidade
Seres Humanos
Indústria Manufatureira/métodos
Indústria Manufatureira/normas
Exposição Ocupacional/efeitos adversos
Exposição Ocupacional/análise
Exposição Ocupacional/prevenção & controle
Medição de Risco/métodos
Medição de Risco/estatística & dados numéricos
Fatores de Risco
Sibéria/epidemiologia
Tempo
Cloreto de Vinil/análise
Cloreto de Vinil/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants, Occupational); 0 (Carcinogens, Environmental); 0R0008Q3JB (Chromium); 18540-29-9 (chromium hexavalent ion); 1HG84L3525 (Formaldehyde); WD06X94M2D (Vinyl Chloride)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180216
[St] Status:MEDLINE


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[PMID]:28985541
[Au] Autor:Wang W
[Ad] Endereço:College of Chemistry and Chemical Engineering, Dezhou University, Dezhou 253023, China. Electronic address: wwqzs@126.com.
[Ti] Título:Chromium (â…¥) removal from aqueous solutions through powdered activated carbon countercurrent two-stage adsorption.
[So] Source:Chemosphere;190:97-102, 2018 Jan.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To exploit the adsorption capacity of commercial powdered activated carbon (PAC) and to improve the efficiency of Cr(VI) removal from aqueous solutions, the adsorption of Cr(VI) by commercial PAC and the countercurrent two-stage adsorption (CTA) process was investigated. Different adsorption kinetics models and isotherms were compared, and the pseudo-second-order model and the Langmuir and Freundlich models fit the experimental data well. The Cr(VI) removal efficiency was >80% and was improved by 37% through the CTA process compared with the conventional single-stage adsorption process when the initial Cr(VI) concentration was 50 mg/L with a PAC dose of 1.250 g/L and a pH of 3. A calculation method for calculating the effluent Cr(VI) concentration and the PAC dose was developed for the CTA process, and the validity of the method was confirmed by a deviation of <5%.
[Mh] Termos MeSH primário: Adsorção
Cromo/isolamento & purificação
Purificação da Água/métodos
[Mh] Termos MeSH secundário: Carcinógenos Ambientais
Carvão Vegetal/química
Cinética
Métodos
Poluentes Químicos da Água/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Carcinogens, Environmental); 0 (Water Pollutants, Chemical); 0R0008Q3JB (Chromium); 16291-96-6 (Charcoal); 18540-29-9 (chromium hexavalent ion)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


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[PMID]:28790062
[Au] Autor:Hughes E
[Ad] Endereço:CMAJ.
[Ti] Título:New evidence of contaminants from fracking.
[So] Source:CMAJ;189(31):E1025-E1026, 2017 08 08.
[Is] ISSN:1488-2329
[Cp] País de publicação:Canada
[La] Idioma:eng
[Mh] Termos MeSH primário: Carcinógenos Ambientais
Água Potável/química
Fraturamento Hidráulico
Poluição Química da Água
[Mh] Termos MeSH secundário: Carcinógenos Ambientais/efeitos adversos
Carcinógenos Ambientais/análise
Água Potável/efeitos adversos
Água Potável/análise
Seres Humanos
Pennsylvania
Poluição Química da Água/efeitos adversos
Poluição Química da Água/análise
[Pt] Tipo de publicação:NEWS
[Nm] Nome de substância:
0 (Carcinogens, Environmental); 0 (Drinking Water)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1503/cmaj.1095459


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[PMID]:28605333
[Au] Autor:Clementino M; Shi X; Zhang Z
[Ad] Endereço:Department of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY 40536.
[Ti] Título:Prevention of Polyphenols Against Carcinogenesis Induced by Environmental Carcinogens.
[So] Source:J Environ Pathol Toxicol Oncol;36(1):87-98, 2017.
[Is] ISSN:2162-6537
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer is one of the major causes of death in humans. Of all cancers, 19% are attributed to exposure to environmental chemical carcinogens. Dietary polyphenols from teas, vegetables, fruits, and many others exhibit multiple activities against cancers. Exposure to environmental carcinogens such as ultraviolet B (UVB), polycyclic aromatic hydrocarbons (PAHs), and heavy metals has been demonstrated to cause cancer in humans. In this article, we specifically select UVB, PAHs, and metals as representative of three types of environmental carcinogens: physical, organic, and inorganic, respectively. We provide a comprehensive review on the role of various dietary polyphenols against carcinogenesis induced by those three types of carcinogens. We summarize the current knowledge of and prospects for prevention of those three groups of carcinogens induced by dietary polyphenols in vitro and in vivo.
[Mh] Termos MeSH primário: Carcinogênese/induzido quimicamente
Carcinogênese/efeitos dos fármacos
Carcinógenos Ambientais/toxicidade
Poluentes Ambientais/toxicidade
Neoplasias/prevenção & controle
Polifenóis/farmacologia
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Dieta
Seres Humanos
Metais Pesados/toxicidade
Hidrocarbonetos Aromáticos Policíclicos/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Carcinogens, Environmental); 0 (Environmental Pollutants); 0 (Metals, Heavy); 0 (Polycyclic Aromatic Hydrocarbons); 0 (Polyphenols); 0 (Protective Agents)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170615
[Lr] Data última revisão:
170615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1615/JEnvironPatholToxicolOncol.2017019057


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[PMID]:28426875
[Au] Autor:Sauer SJ; Tarpley M; Shah I; Save AV; Lyerly HK; Patierno SR; Williams KP; Devi GR
[Ad] Endereço:Department of Surgery, Division of Surgical Sciences, Duke University Medical Sciences, Durham, NC 27710, USA.
[Ti] Título:Bisphenol A activates EGFR and ERK promoting proliferation, tumor spheroid formation and resistance to EGFR pathway inhibition in estrogen receptor-negative inflammatory breast cancer cells.
[So] Source:Carcinogenesis;38(3):252-260, 2017 Mar 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Emerging evidence from epidemiological studies suggests a link between environmental chemical exposure and progression of aggressive breast cancer subtypes. Of all clinically distinct types of breast cancers, the most lethal phenotypic variant is inflammatory breast cancer (IBC). Overexpression of epidermal growth factor receptors (EGFR/HER2) along with estrogen receptor (ER) negativity is common in IBC tumor cells, which instead of a solid mass present as rapidly proliferating diffuse tumor cell clusters. Our previous studies have demonstrated a role of an adaptive response of increased antioxidants in acquired resistance to EGFR-targeting drugs in IBC. Environmental chemicals are known to induce oxidative stress resulting in perturbations in signal transduction pathways. It is therefore of interest to identify chemicals that can potentiate EGFR mitogenic effects in IBC. Herein, we assessed in ER-negative IBC cells a subset of chemicals from the EPA ToxCast set for their effect on EGFR activation and in multiple cancer phenotypic assays. We demonstrated that endocrine-disrupting chemicals such as bisphenol A (BPA) and 2,2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane can increase EGFR/ERK signaling. BPA also caused a corresponding increase in expression of SOD1 and anti-apoptotic Bcl-2, key markers of antioxidant and anti-apoptotic processes. BPA potentiated clonogenic growth and tumor spheroid formation in vitro, reflecting IBC-specific pathological characteristics. Furthermore, we identified that BPA was able to attenuate the inhibitory effect of an EGFR targeted drug in a longer-term anchorage-independent growth assay. These findings provide a potential mechanistic basis for environmental chemicals such as BPA in potentiating a hyperproliferative and death-resistant phenotype in cancer cells by activating mitogenic pathways to which the tumor cells are addicted for survival.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/toxicidade
Carcinógenos Ambientais/toxicidade
Neoplasias Inflamatórias Mamárias/tratamento farmacológico
Fenóis/toxicidade
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Compostos Benzidrílicos/farmacologia
Carcinógenos Ambientais/farmacologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/genética
Receptor alfa de Estrogênio/genética
MAP Quinases Reguladas por Sinal Extracelular/genética
Feminino
Seres Humanos
Neoplasias Inflamatórias Mamárias/genética
Neoplasias Inflamatórias Mamárias/patologia
Estresse Oxidativo/efeitos dos fármacos
Fenóis/farmacologia
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Esferoides Celulares/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Carcinogens, Environmental); 0 (Estrogen Receptor alpha); 0 (Phenols); 0 (estrogen receptor alpha, human); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx003


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[PMID]:28416455
[Au] Autor:Son YO; Pratheeshkumar P; Wang Y; Kim D; Zhang Z; Shi X
[Ad] Endereço:Center for Research on Environmental Disease, College of Medicine, University of Kentucky, 1095 VA Drive, Lexington, KY 40536, USA; National Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 61005, R
[Ti] Título:Protection from Cr(VI)-induced malignant cell transformation and tumorigenesis of Cr(VI)-transformed cells by luteolin through Nrf2 signaling.
[So] Source:Toxicol Appl Pharmacol;331:24-32, 2017 Sep 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cr(VI) is a well known environmental carcinogen, but its mechanism of action and the measures required to mitigate its effects remain to be investigated. Our previous studies showed that exposure of human bronchial epithelial (BEAS-2B) cells to Cr(VI) caused malignant transformation, that these transformed cells progressed through tumorigenesis, and that luteolin, a natural compound, inhibited both of these processes. The present study investigates the underlying mechanisms by which luteolin protects cells against Cr(VI)-induced transformation and tumorigenesis. The present study shows that luteolin activates inducible Nrf2 to inhibit Cr(VI)-generated reactive oxygen species (ROS) in normal BEAS-2B cells. The decreased ROS level is likely responsible for the protective effect of luteolin against Cr(VI)-induced malignant cell transformation in normal cells. By contrast, in cells that have been transformed by Cr(VI), Nrf2 is constitutively activated, and its target proteins, heme oxygenase 1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and superoxide dismutase 1/2 (SOD1/SOD2) are all constitutively activated, and ROS levels are low. Bcl-2, an anti-apoptotic protein and target protein of Nrf2 is elevated. Cr(VI)-transformed BEAS-2B cells develop apoptosis resistance, increasing the survival of these transformed cells. Luteolin decreases interactions between Nrf2 and the antioxidant response element sites of its target anti-apoptotic and antioxidant proteins, Bcl-2, Bcl-XL, and HO-1, which results in decreased constitutive Nrf2 activation. The decreased constitutive Nrf2 activation, decrease in Nrf2 target proteins and consequent apoptosis resistance by luteolin are possible mechanisms that mediate the protective effect of luteolin in Cr(VI)-transformed cells.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Transformação Celular Neoplásica/metabolismo
Cromo/toxicidade
Citoproteção/fisiologia
Luteolina/farmacologia
Fator 2 Relacionado a NF-E2/metabolismo
[Mh] Termos MeSH secundário: Carcinogênese/induzido quimicamente
Carcinogênese/efeitos dos fármacos
Carcinógenos Ambientais/toxicidade
Linhagem Celular
Transformação Celular Neoplásica/efeitos dos fármacos
Citoproteção/efeitos dos fármacos
Relação Dose-Resposta a Droga
Seres Humanos
Fator 2 Relacionado a NF-E2/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens, Environmental); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0R0008Q3JB (Chromium); 18540-29-9 (chromium hexavalent ion); KUX1ZNC9J2 (Luteolin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE


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[PMID]:28408432
[Au] Autor:Dylewska M; Kusmierek JT; Pilzys T; Poznanski J; Maciejewska AM
[Ad] Endereço:Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawinskiego 5A, Warszawa 02-106, Poland.
[Ti] Título:1,N -α-hydroxypropanoadenine, the acrolein adduct to adenine, is a substrate for AlkB dioxygenase.
[So] Source:Biochem J;474(11):1837-1852, 2017 May 16.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1,N -α-hydroxypropanoadenine (HPA) is an exocyclic DNA adduct of acrolein - an environmental pollutant and endocellular oxidative stress product. AlkB dioxygenase belongs to the superfamily of α-ketoglutarate (αKG)- and iron-dependent dioxygenases which remove alkyl lesions from bases via an oxidative mechanism, thereby restoring native DNA structure. Here, we provide and evidence that HPA is mutagenic and is effectively repaired by AlkB dioxygenase. HPA generated in plasmid DNA caused A → C and A → T transversions and, less frequently, A → G transitions. The lesion was efficiently repaired by purified AlkB protein; the optimal pH, Fe(II), and αKG concentrations for this reaction were determined. kinetic data show that the protonated form of HPA is preferentially repaired by AlkB, albeit the reaction is stereoselective. Moreover, the number of reaction cycles carried out by an AlkB molecule remains limited. Molecular modeling of the T(HPA)T/AlkB complex demonstrated that the R stereoisomer in the equatorial conformation of the HPA hydroxyl group is strongly preferred, while the S stereoisomer seems to be susceptible to AlkB-directed oxidative hydroxylation only when HPA adopts the conformation around the glycosidic bond. In addition to the biochemical activity assays, substrate binding to the protein was monitored by differential scanning fluorimetry allowing identification of the active protein form, with cofactor and cosubstrate bound, and monitoring of substrate binding. In contrast FTO, a human AlkB homolog, failed to bind an ssDNA trimer carrying HPA.
[Mh] Termos MeSH primário: Adenina/análogos & derivados
Enzimas AlkB/metabolismo
Carcinógenos Ambientais/metabolismo
Adutos de DNA/metabolismo
Reparo do DNA
Proteínas de Escherichia coli/metabolismo
Modelos Moleculares
Mutagênicos/metabolismo
[Mh] Termos MeSH secundário: Adenina/química
Adenina/metabolismo
Adenina/toxicidade
Enzimas AlkB/química
Enzimas AlkB/genética
Sítios de Ligação
Biocatálise
Carcinógenos Ambientais/química
Carcinógenos Ambientais/toxicidade
Adutos de DNA/química
Adutos de DNA/toxicidade
DNA Bacteriano/química
DNA Bacteriano/efeitos dos fármacos
DNA Bacteriano/metabolismo
Estabilidade Enzimática
Escherichia coli/efeitos dos fármacos
Escherichia coli/crescimento & desenvolvimento
Escherichia coli/metabolismo
Proteínas de Escherichia coli/química
Proteínas de Escherichia coli/genética
Hidroxilação
Conformação Molecular
Simulação de Dinâmica Molecular
Mutagênese/efeitos dos fármacos
Mutagênicos/química
Mutagênicos/toxicidade
Oxirredução
Conformação Proteica
Teoria Quântica
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Estereoisomerismo
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1,N6-alpha-hydroxypropanoadenine); 0 (Carcinogens, Environmental); 0 (DNA Adducts); 0 (DNA, Bacterial); 0 (Escherichia coli Proteins); 0 (Mutagens); 0 (Recombinant Proteins); EC 1.14.11.33 (AlkB Enzymes); JAC85A2161 (Adenine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20161008


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[PMID]:28341215
[Au] Autor:Yim B; Kim H; Kim J; Kim H; Won EJ; Lee YM
[Ad] Endereço:Department of Life Science, College of Natural Sciences, Sangmyung University, Seoul 03016, Republic of Korea.
[Ti] Título:Identification and molecular characterization of cytochrome P450 (CYP450) family genes in the marine ciliate Euplotes crassus: The effect of benzo[a]pyrene and beta-naphthoflavone.
[So] Source:Comp Biochem Physiol C Toxicol Pharmacol;196:71-80, 2017 Jun.
[Is] ISSN:1532-0456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Marine ciliate Euplotes crassus, a single-cell eukaryote, and has been considered as a model organism for monitoring of environmental pollutions in sediments. Cytochrome P450 (CYP450) monooxygenase are phase I enzyme involved in detoxification of environmental pollutants, such as polycyclic aromatic hydrocarbons (PAHs). However, little information on CYP450 family genes in ciliate is available. In the present study, acute toxicity of PAH, benzo[a]pyrene (B[a]P) and PAH-like model compound, beta-naphthoflavone (ß-NF), was investigated; full-length cDNA sequences and genomic structure of five CYP450 genes (CYP5680A1, CYP5681A1, CYP5681B1, CYP5682A1, and CYP5683A1) were analyzed; and finally their activities and transcriptional changes were measured after exposure to PAHs for 48h. According to the results, B[a]P exposure showed a negative effect on E. crassus survival, whereas ß-NF exposure showed no significant effect. The 8h-LC value of B[a]P was determined to be 2.449µM (95%-C.L., 7.726-3.619µM). Five genes belonging to the CYP450 family had conserved domains and clustered with those of ciliate group, as revealed in phylogenetic analysis. CYP activity did not change after exposure to B[a]P, whereas it was slightly, but significantly, induced after exposure to ß-NF. The mRNA expression of five CYP450 genes was significantly modulated in a concentration- and time-dependent manner after exposure to both the chemicals. Our findings suggest that CYP450 genes in E. crassus may be involved in detoxification of B[a]P and ß-NF. This study would give a better understanding about the mode of action of B[a]P and ß-NF in marine ciliates at the molecular level.
[Mh] Termos MeSH primário: Organismos Aquáticos/efeitos dos fármacos
Benzo(a)pireno/toxicidade
Sistema Enzimático do Citocromo P-450/metabolismo
Euplotes/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Poluentes Químicos da Água/toxicidade
beta-Naftoflavona/toxicidade
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Organismos Aquáticos/enzimologia
Carcinógenos Ambientais/toxicidade
Sobrevivência Celular/efeitos dos fármacos
Sequência Conservada
Sistema Enzimático do Citocromo P-450/química
Sistema Enzimático do Citocromo P-450/genética
Euplotes/enzimologia
Euplotes/crescimento & desenvolvimento
Éxons
Íntrons
Cinética
Dose Letal Mediana
Filogenia
Domínios Proteicos
RNA Mensageiro/metabolismo
Alinhamento de Sequência
Análise de Sequência de DNA
Poluentes do Solo/toxicidade
Testes de Toxicidade Aguda
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens, Environmental); 0 (RNA, Messenger); 0 (Soil Pollutants); 0 (Water Pollutants, Chemical); 3417WMA06D (Benzo(a)pyrene); 6051-87-2 (beta-Naphthoflavone); 9035-51-2 (Cytochrome P-450 Enzyme System)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE


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[PMID]:28285017
[Au] Autor:Helle J; Keiler AM; Zierau O; Dörfelt P; Vollmer G; Lehmann L; Chittur SV; Tenniswood M; Welsh J; Kretzschmar G
[Ad] Endereço:Institute of Zoology, Molecular Cell Physiology and Endocrinology, Technische Universität Dresden, 01062, Dresden, Germany.
[Ti] Título:Effects of the aryl hydrocarbon receptor agonist 3-methylcholanthrene on the 17ß-estradiol regulated mRNA transcriptome of the rat uterus.
[So] Source:J Steroid Biochem Mol Biol;171:133-143, 2017 Jul.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Polycyclic aromatic hydrocarbons (PAHs) are products of incomplete combustion of organic compounds, abundant in exhaust fumes and cigarette smoke. They act by binding to the aryl hydrocarbon receptor (AHR) which induces expression of phase 1 and phase 2 enzymes in the liver. PAH induced AHR activation may also lead to adverse effects by modulating other pathways, for example estrogen receptor (ER) signaling in the female reproductive tract. We have investigated the effects of the PAH 3-methylcholanthrene (3-MC) on 17ß-estradiol (E2) dependent signaling in the uterus of ovariectomized rats to characterize the cross talk between AHR and ER on an mRNA transcriptome wide scale. A standard three day uterotrophic assay was performed in young adult Lewis rats. Treatment induced effects were analyzed using histology, immunohistochemistry and gene expression analysis by microarray and qPCR. 3-MC shows broad E2 antagonistic effects on uterine mRNA transcription of the vast majority of E2 regulated genes, significantly altering prostaglandin biosynthesis, complement activation, coagulation pathways and other inflammatory response pathways. The regulation of ER expression in the uterus, but not the regulation of E2 metabolism in the liver, was identified as a potentially important factor in mediating this general antiestrogenic effect. The regulation of prostaglandin biosynthesis by E2 is important for inflammation-like events during pregnancy including the initiation of birth. Our results suggest that adverse effects of PAHs on prostaglandin related pathways are likely caused by the interference with E2 signaling, specifically by inhibiting the E2 mediated downregulation of PGF2α. Characterization of the generalized antagonistic effect of 3-MC on E2 dependent signaling in the rat uterus thus contributes to a better understanding of molecular mechanisms of the toxicity of PAHs in female reproductive organs.
[Mh] Termos MeSH primário: Carcinógenos Ambientais/toxicidade
Estradiol/metabolismo
Moduladores de Receptor Estrogênico/toxicidade
Regulação da Expressão Gênica/efeitos dos fármacos
Metilcolantreno/toxicidade
Receptores de Hidrocarboneto Arílico/agonistas
Útero/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Estradiol/química
Antagonistas de Estrogênios/toxicidade
Feminino
Fígado/citologia
Fígado/efeitos dos fármacos
Fígado/imunologia
Fígado/metabolismo
Especificidade de Órgãos
Ovariectomia
RNA Mensageiro/metabolismo
Distribuição Aleatória
Ratos Endogâmicos Lew
Receptores de Hidrocarboneto Arílico/metabolismo
Receptores Estrogênicos/antagonistas & inibidores
Receptores Estrogênicos/química
Receptores Estrogênicos/genética
Receptores Estrogênicos/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transcriptoma/efeitos dos fármacos
Útero/citologia
Útero/imunologia
Útero/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens, Environmental); 0 (Estrogen Antagonists); 0 (Estrogen Receptor Modulators); 0 (RNA, Messenger); 0 (Receptors, Aryl Hydrocarbon); 0 (Receptors, Estrogen); 4TI98Z838E (Estradiol); 56-49-5 (Methylcholanthrene)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


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[PMID]:28268029
[Au] Autor:Agudelo-Castañeda DM; Teixeira EC; Schneider IL; Lara SR; Silva LF
[Ad] Endereço:Research Group in Environmental Management and Sustainability, Faculty of Environmental Sciences, Universidad De La Costa, Calle 58 #55-66, Barranquilla, Atlántico, 080002, Colombia.
[Ti] Título:Exposure to polycyclic aromatic hydrocarbons in atmospheric PM of urban environments: Carcinogenic and mutagenic respiratory health risk by age groups.
[So] Source:Environ Pollut;224:158-170, 2017 May.
[Is] ISSN:1873-6424
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We investigated the carcinogenic and mutagenic respiratory health risks related to the exposure to atmospheric PAHs in an urban area. Our study focused in the association of these pollutants and their possible effect in human health, principally respiratory and circulatory diseases. Also, we determined a relationship between the inhalation risk of PAHs and meteorological conditions. We validated the hypothesis that in winter PAHs with high molecular weight associated to submicron particles (PM ) may increase exposure risk, especially for respiratory diseases, bronchitis and pneumonia diseases. Moreover, in our study we verified the relationship between diseases and several carcinogenic PAHs (Ind, BbkF, DahA, BaP, and BghiP). These individual PAHs contributed the most to the potential risk of exposure for inhalation of PM . Even at lower ambient concentrations of BaP and DahA in comparison with individual concentrations of other PAHs associated to PM . Mainly, research suggests to include carcinogenic and mutagenic PAHs in future studies of environmental health risk due to their capacity to associate to PM . Such carcinogenic and mutagenic PAHs are likely to provide the majority of the human exposure, since they originate from dense traffic urban areas were humans congregate.
[Mh] Termos MeSH primário: Poluentes Atmosféricos/efeitos adversos
Carcinógenos Ambientais/efeitos adversos
Exposição Ambiental/efeitos adversos
Mutagênicos/efeitos adversos
Material Particulado/química
Hidrocarbonetos Aromáticos Policíclicos/efeitos adversos
Doenças Respiratórias/induzido quimicamente
Saúde da População Urbana/estatística & dados numéricos
[Mh] Termos MeSH secundário: Adulto
Distribuição por Idade
Idoso
Poluentes Atmosféricos/análise
Brasil
Carcinógenos Ambientais/análise
Doenças Cardiovasculares/induzido quimicamente
Doenças Cardiovasculares/epidemiologia
Criança
Cidades
Saúde Ambiental
Monitoramento Ambiental
Cromatografia Gasosa-Espectrometria de Massas
Hospitalização/estatística & dados numéricos
Seres Humanos
Mutagênicos/análise
Tamanho da Partícula
Material Particulado/efeitos adversos
Hidrocarbonetos Aromáticos Policíclicos/análise
Doenças Respiratórias/epidemiologia
Medição de Risco
Estações do Ano
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Carcinogens, Environmental); 0 (Mutagens); 0 (Particulate Matter); 0 (Polycyclic Aromatic Hydrocarbons)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE



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