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[PMID]:28849994
[Au] Autor:Hultman MT; Petersen K; Tollefsen KE
[Ad] Endereço:a Norwegian Institute for Water Research (NIVA) , Oslo , Norway.
[Ti] Título:Characterizing combined effects of antiestrogenic chemicals on vitellogenin production in rainbow trout (Oncorhynchus mykiss) hepatocytes.
[So] Source:J Toxicol Environ Health A;80(16-18):987-1001, 2017.
[Is] ISSN:1528-7394
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fish are exposed to a complex mixture of endocrine disrupting compounds (EDC), some of which display antiestrogenic activity leading to suppression of estrogen receptor (ER)- mediated reproductive processes. Although the main mode of action (MoA) of these antiestrogens is to directly interfere with natural ligand binding of the ER, several other MoA have been proposed. The aim of the present study was to characterize single and combined antiestrogenic effects of the aryl hydrocarbon receptor (AhR)-agonist ß-naphthoflavone (BNF) and ER-antagonist 4-hydroxytamoxifen (OHT) on vitellogenin (Vtg) protein using primary rainbow trout (Oncorhynchus mykiss) hepatocytes. Supporting transcriptional analysis of ER-responsive genes (estrogen receptor-α (er-α), vitellogenin-1 (vtg-1), eggshell zona radiata protein (zrp)) and AhR-mediated genes (aryl hydrocarbon receptor-2ß, cytochrome p450-1a (cyp1a)) was performed by qPCR to characterize the antiestrogenic influence on ER- and AhR-mediated responses. Data demonstrated that both BNF and OHT significantly reduced 17ß-estradiol (E2)-induced Vtg protein expression in a concentration responsive manner, whereas exposure to a mixture of these produced an additive antiestrogenic effect. The results observed at the protein level were further supported by transcriptional analysis of ER-responsive genes (er-α, vtg-1, zrp), where only E2-induced vtg-1 gene expression was significantly decreased by OHT and the mixture of OHT and BNF. E2-induced er-α and zrp gene expression was not markedly altered. The significant reduction of E2-induced vtg-1 gene expression by OHT suggested that the antiestrogenic effect of this compound may be associated with ER signaling pathway. Specific genes involved in putative AhR-ER cross-talk were also investigated, however none were directly associated with the compound anti-estrogenic MoA. Although the MoA of the single compounds and mixture were not completely characterized, the present study enhanced our knowledge of the combined toxicity mediated by antiestrogens acting through different MoA.
[Mh] Termos MeSH primário: Disruptores Endócrinos/toxicidade
Moduladores de Receptor Estrogênico/toxicidade
Hepatócitos/efeitos dos fármacos
Oncorhynchus mykiss/genética
Vitelogeninas/biossíntese
beta-Naftoflavona/toxicidade
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Citocromo P-450 CYP1A1/genética
Citocromo P-450 CYP1A1/metabolismo
Proteínas do Ovo/genética
Proteínas do Ovo/metabolismo
Estradiol/toxicidade
Receptor alfa de Estrogênio/genética
Receptor alfa de Estrogênio/metabolismo
Hepatócitos/metabolismo
Masculino
Oncorhynchus mykiss/metabolismo
Receptores de Hidrocarboneto Arílico/agonistas
Receptores de Hidrocarboneto Arílico/genética
Receptores de Hidrocarboneto Arílico/metabolismo
Receptores Estrogênicos/antagonistas & inibidores
Receptores Estrogênicos/genética
Receptores Estrogênicos/metabolismo
Transdução de Sinais
Tamoxifeno/análogos & derivados
Tamoxifeno/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Egg Proteins); 0 (Endocrine Disruptors); 0 (Estrogen Receptor Modulators); 0 (Estrogen Receptor alpha); 0 (Receptors, Aryl Hydrocarbon); 0 (Receptors, Estrogen); 0 (Vitellogenins); 0 (zona radiata protein, fish); 094ZI81Y45 (Tamoxifen); 17197F0KYM (afimoxifene); 4TI98Z838E (Estradiol); 6051-87-2 (beta-Naphthoflavone); EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1080/15287394.2017.1354435


  2 / 1163 MEDLINE  
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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


  3 / 1163 MEDLINE  
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[PMID]:28110334
[Au] Autor:Liu S; Cheng Y; Rao M; Tang M; Dong Z
[Ad] Endereço:College of Pharmacy, Chongqing Medical University, Chongqing, China.
[Ti] Título:Muscone Induces CYP1A2 and CYP3A4 Enzyme Expression in L02 Human Liver Cells and CYP1A2 and CYP3A11 Enzyme Expression in Kunming Mice.
[So] Source:Pharmacology;99(5-6):205-215, 2017.
[Is] ISSN:1423-0313
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:AIM: To examine the effect of synthetic muscone on the expression of CYP1A2 and CYP3A4 enzymes in human liver L02 cells and in the liver tissue of Kunming mice. METHODS: The L02 hepatic cell line was used to study the effect of low (10-4 µmol/L), middle (10-3 µmol/L), and high concentrations (10-2 µmol/L) of muscone on the expression of CYP1A2 and CYP3A4 enzymes. In addition, the cytochrome P450 (CYP) expression was investigated in Kunming mice after the administration of 10 mg/kg (low), 50 mg/kg (middle), and 100 mg/kg (high) dose of muscone for 6 days. A mixture of phenobarbital (30 mg/kg) and ß-napthoflavone (80 mg/kg) was used as positive control and the effects of the compounds on CYP expression were investigated at the end of 6- and 12-day periods. RESULTS: Muscone induced the expression of CYP1A2 (middle and low concentrations) and of CYP3A4 (high concentration) enzymes in L02 cells. In vivo, administration of muscone in Kunming mice revealed significant weight reduction at the end of 6- and 12-day periods (middle and high doses, respectively), compared to the control group (p < 0.05). Liver toxicity scores indicated that the liver injuries in the positive control and high doses of muscone group were significantly higher in the 6- and 12-day periods, compared to those in the blank control group (p < 0.05). Furthermore, muscone induced CYP1A2 and CYP3A11 expressions in Kunming mice at the middle dose and all doses during the 12-day period as demonstrated by immunoblotting experiments. A low dose of mucone induced the CYP enzyme expression more rapidly, whereas a high dose of muscone caused the longest inductive effect. The results were confirmed by immunohistochemistry experiments and real-time PCR studies, where similar patterns of muscone-mediated inductive effects were noted. CONCLUSIONS: Muscone induces CYP1A2 and CYP3A4 expression in liver cells in vitro and in vivo. In addition, it exhibits liver toxicity in Kunming mice at concentrations higher than 50 mg/kg. The CYP-inductive effect that is caused by muscone encompasses a 6- to 12-day period of activity after drug administration as demonstrated by follow-up in vivo studies.
[Mh] Termos MeSH primário: Cicloparafinas/farmacologia
Citocromo P-450 CYP1A2/biossíntese
Citocromo P-450 CYP3A/biossíntese
Hepatócitos/efeitos dos fármacos
Hepatócitos/enzimologia
Proteínas de Membrana/biossíntese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Indutores do Citocromo P-450 CYP1A2/farmacologia
Indutores do Citocromo P-450 CYP3A/farmacologia
Relação Dose-Resposta a Droga
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Camundongos
Fenobarbital/farmacologia
beta-Naftoflavona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cycloparaffins); 0 (Cytochrome P-450 CYP1A2 Inducers); 0 (Cytochrome P-450 CYP3A Inducers); 0 (Membrane Proteins); 6051-87-2 (beta-Naphthoflavone); EC 1.14.13.67 (CYP3A4 protein, human); EC 1.14.14.1 (CYP1A2 protein, human); EC 1.14.14.1 (Cyp3a11 protein, mouse); EC 1.14.14.1 (Cytochrome P-450 CYP1A2); EC 1.14.14.1 (Cytochrome P-450 CYP3A); UPS3C6CV36 (muscone); YQE403BP4D (Phenobarbital)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170123
[St] Status:MEDLINE
[do] DOI:10.1159/000455154


  4 / 1163 MEDLINE  
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[PMID]:27796684
[Au] Autor:Brauze D; Zawierucha P; Kiwerska K; Bednarek K; Oleszak M; Rydzanicz M; Jarmuz-Szymczak M
[Ad] Endereço:Institute of Human Genetics, Polish Academy of Sciences, Strzeszynska 32, 60-479, Poznan, Poland. brauzdam@man.poznan.pl.
[Ti] Título:Induction of expression of aryl hydrocarbon receptor-dependent genes in human HepaRG cell line modified by shRNA and treated with ß-naphthoflavone.
[So] Source:Mol Cell Biochem;425(1-2):59-75, 2017 Jan.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aryl hydrocarbon receptor (AhR) mediates a variety of biological responses to ubiquitous environmental pollutants. In this study, the effects of administration of ß-naphthoflavone (BNF), a potent AhR ligand, on the expression of AhR-dependent genes were examined by microarray and qPCR analysis in both, differentiated and undifferentiated HepaRG cell lines. To prove that BNF-induced changes of investigated genes were indeed AhR-dependent, we knock down the expression of AhR by stable transfection of HepaRG cells with shRNA. Regardless of genetical identity, our results clearly demonstrate different expression profiles of AhR-dependent genes between differentiated and undifferentiated HepaRG cells. Genes involved in metabolism of xenobiotics constitute only minute fraction of all genes regulated by AhR in HepaRG cells. Participation of AhR in induction of expression of genes associated with regulation of apoptosis or involved in cell proliferation as well as AhR-dependent inhibition of genes connected to cell adhesion could support suggestion of involvement of AhR not only in initiation but also in progression of carcinogenesis. Among the AhR-dependent genes known to be involved in metabolism of xenobiotics, cytochromes P4501A1 and 1B1 belong to the most inducible by BNF. On the contrary, expression of GSTA1 and GSTA2 was significantly inhibited after BNF treatment of HepaRG cells. Among the AhR-dependent genes that are not involved in metabolism of xenobiotics SERPINB2, STC2, ARL4C, and TIPARP belong to the most inducible by BNF. Our results imply involvement of Ah receptor in regulation of CYP19A1, the gene-encoding aromatase, and an enzyme responsible for a key step in the biosynthesis of estrogens.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/biossíntese
Regulação da Expressão Gênica/efeitos dos fármacos
RNA Interferente Pequeno/metabolismo
Receptores de Hidrocarboneto Arílico/biossíntese
beta-Naftoflavona/farmacologia
[Mh] Termos MeSH secundário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Adesão Celular/efeitos dos fármacos
Linhagem Celular
Estrogênios/biossíntese
Estrogênios/genética
Seres Humanos
RNA Interferente Pequeno/genética
Receptores de Hidrocarboneto Arílico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AHR protein, human); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Estrogens); 0 (RNA, Small Interfering); 0 (Receptors, Aryl Hydrocarbon); 6051-87-2 (beta-Naphthoflavone)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-016-2862-3


  5 / 1163 MEDLINE  
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[PMID]:27821351
[Au] Autor:Ferreira RS; Chivittz CD; Santos GS; Zanette J
[Ad] Endereço:Instituto de Ciências Biológicas (ICB), Universidade Federal do Rio Grande (FURG), Rio Grande, RS 96203-900, Brazil; Programa de Pós-graduação em Biologia de Ambientes Aquáticos Continentais (PPGBAC), Universidade Federal do Rio Grande (FURG), Rio Grande, RS 96203-900, Brazil.
[Ti] Título:Cytochrome P450 1A mRNA in the guppy Phalloceros caudimaculatus and response to beta-naphthoflavone and environmental samples.
[So] Source:Aquat Toxicol;181:86-93, 2016 Dec.
[Is] ISSN:1879-1514
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The cytochrome P450 1A (CYP1A) mRNA is induced by environmental contaminants such as PAHs, PCBs and dioxins. The present study cloned the CYP1A transcript from the guppy Phalloceros caudimaculatus, which represents a potential fish for toxicological studies in South America. The newly identified CYP1A encodes a protein with 521 amino acids that shared 96-70% identity with other fishes. The characterization of organ- and time-dependent induction of CYP1A using RT-qPCR was evaluated after waterborne exposure to beta-naphthoflavone (BNF; 1µM). The minimum exposure time that elicited significant CYP1A induction was 1h for liver, gill, gut, brain, anal fin and fingerlings; 2h for dorsal fin; and 4h for kidney and tail fin. CYP1A tended to reach peak induction in the first few hours (4h-8h) of experiment in most organs, although levels remained induced until the end of the experiment (96h). Validation of CYP1A use in environmental sample was performed by exposing P. caudimaculatus to elutriate made from sediment of three streams located in adjacent areas of the Patos Lagoon Estuary (RS, Brazil). CYP1A in liver, gills and anal fin was induced by elutriate made from urban (S1) and industrial (S2) sites; and not induced by a reference site located 22 Km from potential contaminant sources, suggesting that environmental contamination plays a role in this induction. The results suggest that fins could be used for CYP1A biomarker analysis and employed in non-lethal biopsy methods for environmental monitoring. The responsiveness of the newly identified CYP1A to BNF and elutriate indicates that the guppy P. caudimaculatus could be used for environmental toxicology investigations in South American environments.
[Mh] Termos MeSH primário: Citocromo P-450 CYP1A1/metabolismo
Poecilia/metabolismo
RNA Mensageiro/metabolismo
Poluentes Químicos da Água/toxicidade
beta-Naftoflavona/toxicidade
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Nadadeiras de Animais/efeitos dos fármacos
Nadadeiras de Animais/metabolismo
Animais
Biomarcadores/metabolismo
Citocromo P-450 CYP1A1/química
Citocromo P-450 CYP1A1/genética
Monitoramento Ambiental
Proteínas de Peixes/genética
Proteínas de Peixes/metabolismo
Brânquias/efeitos dos fármacos
Brânquias/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Dados de Sequência Molecular
Poecilia/crescimento & desenvolvimento
Alinhamento de Sequência
Poluentes Químicos da Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fish Proteins); 0 (RNA, Messenger); 0 (Water Pollutants, Chemical); 6051-87-2 (beta-Naphthoflavone); EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161109
[St] Status:MEDLINE


  6 / 1163 MEDLINE  
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[PMID]:27594096
[Au] Autor:Mahiout S; Pohjanvirta R
[Ad] Endereço:Department of Food Hygiene and Environmental Health, Faculty of Veterinary Medicine, University of Helsinki, Mustialankatu 1, FI-00790 Helsinki, Finland. Electronic address: selma.mahiout@helsinki.fi.
[Ti] Título:Aryl hydrocarbon receptor agonists trigger avoidance of novel food in rats.
[So] Source:Physiol Behav;167:49-59, 2016 Dec 01.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the toxicity of dioxins, but also plays important physiological roles, which are only beginning to unfold. Previous studies have surprisingly unveiled that low doses of the potent AHR agonist TCDD induce a strong and persistent avoidance of novel food items in rats. Here, we further examined the involvement of the AHR in the avoidance response in Sprague-Dawley rats with three established AHR agonists: 6-formylindolo(3,2-b)carbazole (FICZ), ß-naphthoflavone (BNF) and benzo[a]pyrene (BaP); with a novel selective AHR modulator (C2); and with an activator of another nuclear receptor, CAR: 2,4,6-tryphenyldioxane-1,3 (TPD). As sensitive indices of AHR or CAR activity, we used Cyp1a1 and Cyp2b1 gene expression, as they are, respectively, the drug-metabolizing enzymes specifically regulated by them. We further attempted to address the roles played by enhanced neophobia and conditioned taste aversion (CTA) in the avoidance behaviour. All AHR agonists triggered practically total avoidance of novel chocolate, but the durations varied. Likewise, acutely subtoxic doses of C2, differing by 25-fold, all elicited a similar outcome. In contrast, TPD did not influence chocolate consumption at all. If rats were initially accustomed to chocolate for 6h after single FICZ or BNF exposure, avoidance was still clearly present two weeks later when chocolate was offered again. Hence, the avoidance response appears to specifically involve the AHR instead of being triggered by induction of intestinal or hepatic nuclear receptor signalling in general. It is also shared by both endogenous and exogenous AHR activators. Moreover, this behavioural change in rats seems to contain elements of both CTA and enhanced neophobia, but further clarification of this is still required.
[Mh] Termos MeSH primário: Aprendizagem da Esquiva/efeitos dos fármacos
Comportamento Alimentar/efeitos dos fármacos
Preferências Alimentares/efeitos dos fármacos
Receptores de Hidrocarboneto Arílico/agonistas
Paladar/efeitos dos fármacos
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Benzo(a)pireno/metabolismo
Benzo(a)pireno/farmacologia
Carbazóis/farmacologia
Citocromo P-450 CYP1A1/genética
Citocromo P-450 CYP1A1/metabolismo
Citocromo P-450 CYP2B1/genética
Citocromo P-450 CYP2B1/metabolismo
Relação Dose-Resposta a Droga
Ingestão de Alimentos/efeitos dos fármacos
Masculino
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Receptores de Hidrocarboneto Arílico/metabolismo
Fatores de Tempo
beta-Naftoflavona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-formylindolo(3,2-b)carbazole); 0 (Carbazoles); 0 (RNA, Messenger); 0 (Receptors, Aryl Hydrocarbon); 3417WMA06D (Benzo(a)pyrene); 6051-87-2 (beta-Naphthoflavone); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 1.14.14.1 (Cytochrome P-450 CYP2B1)
[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:160906
[St] Status:MEDLINE


  7 / 1163 MEDLINE  
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[PMID]:27490210
[Au] Autor:Fu G; Zhou C; Wang Y; Fang W; Zhou J; Zhao S; Ma L
[Ad] Endereço:East China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Key Laboratory of East China Sea and Oceanic Fishery Resources Exploitation and Utilization, Ministry of Agriculture, 300 Jungong Road, Shanghai, 200090, China.
[Ti] Título:Effects of inducers of cytochrome P450s on enrofloxacin N-deethylation in crucian carp Carassius auratus gibelio.
[So] Source:Environ Toxicol Pharmacol;46:188-193, 2016 Sep.
[Is] ISSN:1872-7077
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In this study with crucian carp (Carassius auratus gibelio), the effect on enrofloxacin (EF) and its metabolite ciprofloxacin (CF) and on the activity of cytochrome P450 1A (CYP1A) and cytochrome P450 3A (CYP3A) was estimated following the oral administration of rifampicin (RIF) (12mg/kg) and ß-naphthoflavone (BNF) (12mg/kg), respectively. First, reversed-phase high-performance liquid chromatography (RP-HPLC) was used to detect the pharmacokinetics of EF with continual blood sampling. In RIF-treated, BNF-treated and control groups, the value of the CmaxCF/CmaxEF ratio was 4.41, 0.81 and 0.95, and the corresponding value of the AUC0-t-CF/AUC0-t-EF ratio was 3.69, 1.84 and 1.76, respectively. In the RIF-treated, BNF-treated and control groups, the MRT values of EF were 26.57, 27.45 and 30.88h, and the corresponding values for CF were 5.79, 35.18 and 38.11h, respectively. Based on these results for crucian carp, the accumulation and elimination of EF and CF in the RIF-treated group were more rapid than in BNF-treated and control groups. Second, liver microsomes were pretreated with the inducer of CYP1A for BNF and that of CYP3A for RIF, and then the enzymatic activities of CYP1A and CYP3A were measured, respectively. The activities of ethoxyresorufin-O-deethylation (EROD) and erythromycin-N-demethylation (ERND) increased significantly (P<0.05) for CYP1A and CYP3A, respectively. However, in further experiments on the formation of CF, the level of EF N-deethylation was significantly induced by RIF and inhibited by ketoconazole (KTZ) for CYP3A but had no influence for CYP1A, BNF and berberine chloride (BER). We concluded that CYP3A might be responsible for the N-deethylation of EF and because of this activity, could also serve as a toxicity biomarker in crucian carp.
[Mh] Termos MeSH primário: Antibacterianos/farmacocinética
Indutores das Enzimas do Citocromo P-450/farmacologia
Fluoroquinolonas/farmacocinética
Carpa Dourada/metabolismo
Microssomos Hepáticos/enzimologia
[Mh] Termos MeSH secundário: Animais
Antibacterianos/sangue
Citocromo P-450 CYP1A1/metabolismo
Citocromo P-450 CYP3A/metabolismo
Interações Medicamentosas
Fluoroquinolonas/sangue
Carpa Dourada/sangue
Microssomos Hepáticos/efeitos dos fármacos
Rifampina/farmacologia
beta-Naftoflavona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Cytochrome P-450 Enzyme Inducers); 0 (Fluoroquinolones); 3DX3XEK1BN (enrofloxacin); 6051-87-2 (beta-Naphthoflavone); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 1.14.14.1 (Cytochrome P-450 CYP3A); VJT6J7R4TR (Rifampin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170812
[Lr] Data última revisão:
170812
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160805
[St] Status:MEDLINE


  8 / 1163 MEDLINE  
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[PMID]:27402199
[Au] Autor:Kimura M; Mizukami S; Watanabe Y; Onda N; Yoshida T; Shibutani M
[Ad] Endereço:Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology, 3-5-8 Saiwai-cho, Fuchu-shi, Tokyo 183-8509, Japan; Pathogenetic Veterinary Science, United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, Gifu-shi, Gifu 501-1193, Japan.
[Ti] Título:Aberrant cell cycle regulation in rat liver cells induced by post-initiation treatment with hepatocarcinogens/hepatocarcinogenic tumor promoters.
[So] Source:Exp Toxicol Pathol;68(7):399-408, 2016 Aug.
[Is] ISSN:1618-1433
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The present study aimed to determine the onset time of hepatocarcinogen/hepatocarcinogenic tumor promoter-specific cell proliferation, apoptosis and aberrant cell cycle regulation after post-initiation treatment. Six-week-old rats were treated with the genotoxic hepatocarcinogen, carbadox (CRB), the marginally hepatocarcinogenic leucomalachite green (LMG), the tumor promoter, ß-naphthoflavone (BNF) or the non-carcinogenic hepatotoxicant, acetaminophen, for 2, 4 or 6 weeks during the post-initiation phase using a medium-term liver bioassay. Cell proliferation activity, expression of G2 to M phase- and spindle checkpoint-related molecules, and apoptosis were immunohistochemically analyzed at week 2 and 4, and tumor promotion activity was assessed at week 6. At week 2, hepatocarcinogen/tumor promoter-specific aberrant cell cycle regulation was not observed. At week 4, BNF and LMG increased cell proliferation together with hepatotoxicity, while CRB did not. Additionally, BNF and CRB reduced the number of cells expressing phosphorylated-histone H3 in both ubiquitin D (UBD)(+) cells and Ki-67(+) proliferating cells, suggesting development of spindle checkpoint dysfunction, regardless of cell proliferation activity. At week 6, examined hepatocarcinogens/tumor promoters increased preneoplastic hepatic foci expressing glutathione S-transferase placental form. These results suggest that some hepatocarcinogens/tumor promoters increase their toxicity after post-initiation treatment, causing regenerative cell proliferation. In contrast, some genotoxic hepatocarcinogens may disrupt the spindle checkpoint without facilitating cell proliferation at the early stage of tumor promotion. This suggests that facilitation of cell proliferation and disruption of spindle checkpoint function are induced by different mechanisms during hepatocarcinogenesis. Four weeks of post-initiation treatment may be sufficient to induce hepatocarcinogen/tumor promoter-specific cellular responses.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Carcinógenos/toxicidade
Proliferação Celular/efeitos dos fármacos
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Fígado/efeitos dos fármacos
Pontos de Checagem da Fase M do Ciclo Celular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetaminofen/toxicidade
Animais
Carbadox/toxicidade
Cocarcinogênese
Dietilnitrosamina/toxicidade
Imuno-Histoquímica
Antígeno Ki-67/metabolismo
Fígado/metabolismo
Fígado/patologia
Masculino
Ratos Endogâmicos F344
Corantes de Rosanilina/toxicidade
Fatores de Tempo
beta-Naftoflavona/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carcinogens); 0 (Ki-67 Antigen); 0 (Rosaniline Dyes); 362O9ITL9D (Acetaminophen); 3IQ78TTX1A (Diethylnitrosamine); 6051-87-2 (beta-Naphthoflavone); 8U61G37Z20 (leucomalachite green); M2X04R2E2Y (Carbadox)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170206
[Lr] Data última revisão:
170206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE


  9 / 1163 MEDLINE  
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[PMID]:27062342
[Au] Autor:Li MH
[Ad] Endereço:Environmental Toxicology Laboratory, Department of Geography, National Taiwan University, 1, Section 4, Roosevelt Road, Taipei 106, Taiwan. Electronic address: meihuili@ntu.edu.tw.
[Ti] Título:Development of in vivo biotransformation enzyme assays for ecotoxicity screening: In vivo measurement of phases I and II enzyme activities in freshwater planarians.
[So] Source:Ecotoxicol Environ Saf;130:19-28, 2016 Aug.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The development of a high-throughput tool is required for screening of environmental pollutants and assessing their impacts on aquatic animals. Freshwater planarians can be used in rapid and sensitive toxicity bioassays. Planarians are known for their remarkable regeneration ability but much less known for their metabolic and xenobiotic biotransformation abilities. In this study, the activities of different phase I and II enzymes were determined in vivo by directly measuring fluorescent enzyme substrate disappearance or fluorescent enzyme metabolite production in planarian culture media. For phase I enzyme activity, O-deethylation activities with alkoxyresorufin could not be detected in planarian culture media. By contrast, O-deethylation activities with alkoxycoumarin were detected in planarian culture media. Increases in 7-ethoxycoumarin O-deethylase (ECOD) activities was only observed in planarians exposed to 1µM, but not 10µM, ß-naphthoflavone for 24h. ECOD activity was inhibited in planarians exposed to 10 and 100µM rifampicin or carbamazepine for 24h. For phase II enzyme activity, DT-diaphorase, arylsulfatases, uridine 5'-diphospho (UDP)-glucuronosyltransferase or catechol-O-methyltransferase activity was determined in culture media containing planarians. The results of this study indicate that freshwater planarians are a promising model organism to monitor exposure to environmental pollutants or assess their impacts through the in vivo measurement of phase I and II enzyme activities.
[Mh] Termos MeSH primário: Ensaios Enzimáticos
Planárias/efeitos dos fármacos
Planárias/enzimologia
[Mh] Termos MeSH secundário: O-Dealquilase 7-Alcoxicumarina/metabolismo
Animais
Biotransformação
Catecol O-Metiltransferase/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Monitoramento Ambiental/métodos
Água Doce
Modelos Biológicos
Poluentes Químicos da Água/metabolismo
Poluentes Químicos da Água/toxicidade
Xenobióticos/metabolismo
Xenobióticos/toxicidade
beta-Naftoflavona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Water Pollutants, Chemical); 0 (Xenobiotics); 6051-87-2 (beta-Naphthoflavone); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.13.- (7-Alkoxycoumarin O-Dealkylase); EC 2.1.1.6 (Catechol O-Methyltransferase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160411
[St] Status:MEDLINE


  10 / 1163 MEDLINE  
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[PMID]:27041667
[Au] Autor:Holen E; Olsvik PA
[Ad] Endereço:National Institute of Nutrition and Seafood Research (NIFES), P. B. 2029 Nordnes, 5817, Bergen, Norway. Electronic address: eho@nifes.no.
[Ti] Título:ß-naphthoflavone interferes with cyp1c1, cox2 and IL-8 gene transcription and leukotriene B4 secretion in Atlantic cod (Gadus morhua) head kidney cells during inflammation.
[So] Source:Fish Shellfish Immunol;54:128-34, 2016 Jul.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to evaluate how ß-naphthoflavone interacts with lipopolysaccharide (LPS) and polyinosinic acid: polycytidylic acid (poly I: C) induced innate immune parameters as well as phase I and phase II detoxification enzymes in head kidney cells isolated from Atlantic cod. ß-naphthoflavone is a pure agonist of aryl hydrocarbon receptor (AhR) while LPS and poly I: C are not. ß-naphthoflavone was added to head kidney leukocytes alone or together with LPS or poly I: C and the responses were evaluated in terms of protein and gene expression. The results showed that ß-naphthoflavone (25 nM), with and without LPS, significantly induced cytochrome P450 (cyp1c) transcription in cod head kidney cells. ß-naphthoflavone (100 nM) in the presence of the virus mimic, poly I: C, also increased cyp1c1transcription. LPS induced cyp1c1, cyclooxygenase 2 (cox2), interleukin 1ß (IL-1ß), interleukin 6 (IL-6) and interleukin 8 (IL-8) transcription, genes that were not affected by the tested ß-naphthoflavone concentrations alone. However, ß-naphthoflavone (25 and 50 nM) strengthened LPS induced cox2 and IL-8 transcription. Cod head kidney cells exposed to ß-naphthoflavone concentrations ranging from 25 to 100 nM, with and without LPS or poly I: C, expressed AhR protein. LPS or ß-naphthoflavone (5-50 nM) significantly induced leukotriene B4 (LTB4) secretion compared to control. In conclusion, this study suggests that ß-naphthoflavone could interfere with LPS induced immune cell signaling in cod head kidney cells.
[Mh] Termos MeSH primário: Inibidores Enzimáticos/toxicidade
Proteínas de Peixes/genética
Gadus morhua/genética
Inflamação
Leucotrieno B4/secreção
Transcrição Genética/efeitos dos fármacos
beta-Naftoflavona/toxicidade
[Mh] Termos MeSH secundário: Animais
Proteínas de Peixes/metabolismo
Gadus morhua/imunologia
Gadus morhua/metabolismo
Rim Cefálico/efeitos dos fármacos
Rim Cefálico/metabolismo
Imunidade Inata
Leucócitos/efeitos dos fármacos
Leucócitos/metabolismo
Lipopolissacarídeos/farmacologia
Desentoxicação Metabólica Fase I
Desintoxicação Metabólica Fase II
Poli I-C/farmacologia
Pseudomonas aeruginosa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Fish Proteins); 0 (Lipopolysaccharides); 1HGW4DR56D (Leukotriene B4); 6051-87-2 (beta-Naphthoflavone); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160405
[St] Status:MEDLINE



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