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[PMID]:29061807
[Au] Autor:Sheikh IA; Beg MA; Yasir M
[Ad] Endereço:King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia iasheikh@kau.edu.sa.
[Ti] Título:Molecular Interactions of Carcinogenic Aromatic Amines, 4-Aminobiphenyl and 4,4'-Diaminobiphenyl, with Lactoperoxidase - Insight to Breast Cancer.
[So] Source:Anticancer Res;37(11):6245-6249, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Lactoperoxidase (LPO) is an antimicrobial protein present in milk, saliva, gastric secretions, tears and upper respiratory tract secretions. LPO constitutes an important enzyme of the human immune defense system. However, LPO has also been suggested to be involved in breast cancer etiology through production of reactive free radicals and activation of carcinogenic aromatic compounds. Aromatic compounds are generally highly lipophilic and thus accumulate in highly fatty breast tissues. The aromatic compounds 4-aminobiphenyl (ABP) and 4,4'-diaminobiphenyl (BZ) are known to have carcinogenic properties. LPO catalyzes their oxidation and converts them into reactive products which bind to DNA and form adducts. These DNA adducts subsequently lead to breast cancer. MATERIALS AND METHODS: The crystal structure of LPO was obtained from Protein Data Bank. Structures of ABP and BZ were retrieved from PubChem database. Induced Fit Docking was performed using glide module from Schrodinger. RESULTS: The present study reports the structural binding of ABP and BZ with LPO using in silico approaches. The amino acid residues of LPO involved in the binding with the two aromatic ligands were characterized and binding energy values were calculated. CONCLUSION: Both ABP and BZ were placed in the substrate binding site present in the distal heme cavity of LPO with good affinity. The binding mode mimicked that of the natural substrate since these compounds did not disturb the water molecule that plays an important role in the oxidation reaction. Thus, the water molecule is potentially available for facilitating the subsequent activation of the aromatic amines to reactive species which may form DNA adducts leading to breast cancer.
[Mh] Termos MeSH primário: Compostos de Aminobifenil/metabolismo
Neoplasias da Mama/induzido quimicamente
Carcinógenos/metabolismo
Adutos de DNA/metabolismo
Radicais Livres/química
Lactoperoxidase/metabolismo
[Mh] Termos MeSH secundário: Compostos de Aminobifenil/efeitos adversos
Compostos de Aminobifenil/química
Sítios de Ligação
Neoplasias da Mama/enzimologia
Carcinógenos/química
Adutos de DNA/efeitos adversos
Adutos de DNA/química
Feminino
Seres Humanos
Lactoperoxidase/química
Modelos Moleculares
Simulação de Acoplamento Molecular
Estrutura Molecular
Oxirredução
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Carcinogens); 0 (DNA Adducts); 0 (Free Radicals); 16054949HJ (4-biphenylamine); EC 1.11.1.- (Lactoperoxidase)
[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:171025
[St] Status:MEDLINE


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[PMID]:28493705
[Au] Autor:Cai T; Bellamri M; Ming X; Koh WP; Yu MC; Turesky RJ
[Ti] Título:Quantification of Hemoglobin and White Blood Cell DNA Adducts of the Tobacco Carcinogens 2-Amino-9H-pyrido[2,3-b]indole and 4-Aminobiphenyl Formed in Humans by Nanoflow Liquid Chromatography/Ion Trap Multistage Mass Spectrometry.
[So] Source:Chem Res Toxicol;30(6):1333-1343, 2017 Jun 19.
[Is] ISSN:1520-5010
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aromatic amines covalently bound to hemoglobin (Hb) as sulfinamide adducts at the cysteine 93 residue of the Hb ß chain have served as biomarkers to assess exposure to this class of human carcinogens for the past 30 years. In this study, we report that 2-amino-9H-pyrido[2,3-b]indole (AαC), an abundant carcinogenic heterocyclic aromatic amine formed in tobacco smoke and charred cooked meats, also reacts with Hb to form a sulfinamide adduct. A novel nanoflow liquid chromatography/ion trap multistage mass spectrometry (nanoLC-IT/MS ) method was established to assess exposure to AαC and the tobacco-associated bladder carcinogen 4-aminobiphenyl (4-ABP) through their Hb sulfinamide adducts. Following mild acid hydrolysis of Hb in vitro, the liberated AαC and 4-ABP were derivatized with acetic anhydride to form the N-acetylated amines, which were measured by nanoLC-IT/MS . The limits of quantification (LOQ) for AαC- and 4-ABP-Hb sulfinamide adducts were ≤7.1 pg/g Hb. In a pilot study, the mean level of Hb sulfinamide adducts of AαC and 4-ABP were, respectively, 3.4-fold and 4.8-fold higher in smokers (>20 cigarettes/day) than nonsmokers. In contrast, the major DNA adducts of 4-ABP, N-(2'-deoxyguanosin-8-yl)-4-aminobiphenyl, and AαC, N-(2'-deoxyguanosin-8-yl)-2-amino-9H-pyrido[2,3-b]indole, were below the LOQ (3 adducts per 10 bases) in white blood cell (WBC) DNA of smokers and nonsmokers. These findings reaffirm that tobacco smoke is a major source of exposure to AαC. Hb sulfinamide adducts are suitable biomarkers to biomonitor 4-ABP and AαC; however, neither carcinogen binds to DNA in WBC, even in heavy smokers, at levels sufficient for biomonitoring.
[Mh] Termos MeSH primário: Compostos de Aminobifenil/química
Carbolinas/química
Carcinógenos/química
Adutos de DNA/análise
Hemoglobinas/química
Leucócitos/metabolismo
Tabaco/química
[Mh] Termos MeSH secundário: Cromatografia Líquida de Alta Pressão
Adutos de DNA/química
Hemoglobinas/análise
Seres Humanos
Espectrometria de Massas
Estrutura Molecular
Nanotecnologia
Sulfamerazina/análise
Sulfamerazina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Carbolines); 0 (Carcinogens); 0 (DNA Adducts); 0 (Hemoglobins); 0 (sulfenamide); 16054949HJ (4-biphenylamine); P0GZ1ICS6X (2-amino-9H-pyrido(2,3-b)indole); UR1SAB295F (Sulfamerazine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1021/acs.chemrestox.7b00072


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[PMID]:28112906
[Au] Autor:Huang Q; Xie J; Liu Y; Zhou A; Li J
[Ad] Endereço:Department of Biomedical Polymers and Artificial Organs, College of Polymer Science and Engineering, State Key Laboratory of Polymer Materials Engineering, Sichuan University , Chengdu 610065, China.
[Ti] Título:Detecting the Formation and Transformation of Oligomers during Insulin Fibrillation by a Dendrimer Conjugated with Aggregation-Induced Emission Molecule.
[So] Source:Bioconjug Chem;28(4):944-956, 2017 Apr 19.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The fibrillation of protein is harmful and impedes the use of protein drugs. It also relates to various debilitating diseases such as Alzheimer's diseases. Thus, investigating the protein fibrillation process is necessary. In this study, poly(amido amine) dendrimers (PAMAM) of generation 3 (G3) and generation 4 (G4) were synthesized and conjugated with 4-aminobiphenyl, an aggregation-induced emission (AIE) moiety, at varied grafting ratios. Among them, one fluorescence probe named G3-biph-3 that was grafted average 3.25 4-aminobiphenyl to the G3, can detect the transformations both from native insulin to oligomers and from oligomers to fibrils. The size difference of native insulin, oligomers, and fibrils was proposed to be the main factor leading to the detection of the above transformations. Different molecular weights of sodium polyacrylate (PAAS) were also applied as a model to interact with G3-biph-3 to further reveal the mechanism. The results indicated that PAMAM with a certain generation and grafted with appropriate AIE groups can detect the oligomer formation and transformation during the insulin fibrillation process.
[Mh] Termos MeSH primário: Amiloide/química
Dendrímeros/química
Corantes Fluorescentes/química
Insulina/química
[Mh] Termos MeSH secundário: Resinas Acrílicas/química
Compostos de Aminobifenil/química
Amiloide/ultraestrutura
Animais
Agregados Proteicos
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acrylic Resins); 0 (Aminobiphenyl Compounds); 0 (Amyloid); 0 (Dendrimers); 0 (Fluorescent Dyes); 0 (Insulin); 0 (PAMAM Starburst); 0 (Protein Aggregates); 16054949HJ (4-biphenylamine); 4Q93RCW27E (carbopol 940)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE
[do] DOI:10.1021/acs.bioconjchem.6b00665


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[PMID]:28027837
[Au] Autor:Bie Z; Lu W; Zhu Y; Chen Y; Ren H; Ji L
[Ad] Endereço:Quality Supervision & Test Center, China National Tobacco Corporation Shandong Branch, Jinan 250098, China.
[Ti] Título:Rapid determination of six carcinogenic primary aromatic amines in mainstream cigarette smoke by two-dimensional online solid phase extraction combined with liquid chromatography tandem mass spectrometry.
[So] Source:J Chromatogr A;1482:39-47, 2017 Jan 27.
[Is] ISSN:1873-3778
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A fully automated, rapid, and reliable method for simultaneous determination of six carcinogenic primary aromatic amines (AAs), including o-toluidine (o-TOL), 2, 6-dimethylaniline (2, 6-DMA), o-anisidine (o-ASD), 1-naphthylamine (1-ANP), 2-naphthylamine (2-ANP), and 4-aminobiphenyl (4-ABP), in mainstream cigarette smoke was established. The proposed method was based on two-dimensional online solid phase extraction combined with liquid chromatography tandem mass spectrometry (SPE/LC-MS/MS). The particulate phase of the mainstream cigarette smoke was collected on a Cambridge filter pad and pretreated via ultrasonic extraction with 2% formic acid (FA), while the gas phase was trapped by 2% FA without pretreatment for determination. The two-dimensional online SPE comprised of two cartridges with different absorption characteristics was applied for sample pretreatment. Analysis was performed by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) under multiple reaction monitoring mode. Each sample required about 0.5h for solid phase extraction and analysis. The limit of detections (LODs) for six AAs ranged from 0.04 to 0.58ng/cig and recoveries were within 84.5%-122.9%. The relative standard deviations of intra- and inter-day tests for 3R4F reference cigarette were less than 6% and 7%, respectively, while no more than 7% and 8% separately for a type of Virginia cigarette. The proposed method enabled minimum sample pretreatment, full automation, and high throughput with high selectivity, sensitivity, and accuracy. As a part of the validation procedure, fifteen brands of cigarettes were tested by the designed method.
[Mh] Termos MeSH primário: Carcinógenos/análise
Fumaça/análise
Extração em Fase Sólida/métodos
Espectrometria de Massas em Tandem/métodos
Tabaco/química
[Mh] Termos MeSH secundário: 1-Naftilamina/análise
Compostos de Aminobifenil/análise
Compostos de Anilina/análise
Cromatografia Líquida
Limite de Detecção
Produtos do Tabaco/classificação
Toluidinas/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Aniline Compounds); 0 (Carcinogens); 0 (Smoke); 0 (Toluidines); 16054949HJ (4-biphenylamine); 4FT62OX08D (2,6-xylidine); 9753I242R5 (1-Naphthylamine); B635MZ0ZLU (2-toluidine); NUX042F201 (2-anisidine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161229
[St] Status:MEDLINE


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[PMID]:27746196
[Au] Autor:Hanna D; Riedmaier AE; Sugamori KS; Grant DM
[Ad] Endereço:Department of Pharmacology & Toxicology, Faculty of Medicine, University of Toronto,1 King's College Circle, Toronto M5S 1A8, Canada.
[Ti] Título:Influence of sex and developmental stage on acute hepatotoxic and inflammatory responses to liver procarcinogens in the mouse.
[So] Source:Toxicology;373:30-40, 2016 Dec 12.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The incidence of liver cancer is higher in men than in women. This sex difference is also observed in murine tumor induction models that result in the appearance of liver tumors in adult mice following their exposure on postnatal days 8 and/or 15 to carcinogens such as 4-aminobiphenyl (ABP) or diethylnitrosamine (DEN). Previous studies performed in adult mice showed that acute hepatotoxic and inflammatory responses to high-dose DEN exposure were greater in males than in females, leading to the suggestion that these responses could account for the sex difference in tumor development. We also recently observed that female but not male mice exposed postnatally to ABP had slightly increased expression of the antioxidant defense genes Nqo1 and Ggt1, which are regulated by the oxidative stress response protein nuclear factor erythroid 2-related factor 2 (NRF2), while expression of Hmox1 was increased in both sexes. The goal of the present study was therefore to compare selected acute hepatotoxic, inflammatory and oxidative stress defense responses to ABP, DEN, or the prototype hepatotoxicant carbon tetrachloride (CCl ), in male and female mice exposed to these chemicals either postnatally or as adults. Exposure of adult mice to ABP, DEN or CCl produced a 2-fold greater acute elevation in serum levels of the hepatotoxicity biomarker alanine aminotransferase (ALT) in males than in females, while levels of the inflammatory biomarker interleukin-6 (IL-6) showed no sex difference. However, treatment of immature mice with either ABP or DEN using standard tumor-inducing postnatal exposure protocols produced no increase in serum ALT or IL-6 levels in either males or females, while CCl produced a 40-fold ALT elevation but with no sex difference. Basal expression of the NRF2-responsive gene Nqo1 was higher in adult females than in males, but there was no sex difference in basal expression of Ggt1 or Hmox1. Sexually immature animals showed no sex difference in basal expression of any of the three genes. Postnatal DEN exposure modestly increased the expression of Ggt1 only in male mice and Nqo1 in both sexes, while CCl slightly increased expression of Ggt1 in both males and females and Nqo1 only in females. Taken together, our results make it unlikely that acute hepatotoxic, inflammatory or NRF2-activated gene responses account for the male predominance in liver tumor growth following postnatal carcinogen exposure in mice. Our findings also suggest that acute toxicity studies performed in adult mice should be interpreted with caution when extrapolating potential mechanisms to liver carcinogenesis models that commonly use postnatally exposed mice.
[Mh] Termos MeSH primário: Carcinógenos/toxicidade
Doença Hepática Induzida por Substâncias e Drogas/patologia
Inflamação/induzido quimicamente
Inflamação/patologia
Neoplasias Hepáticas/induzido quimicamente
Neoplasias Hepáticas/patologia
[Mh] Termos MeSH secundário: Envelhecimento/fisiologia
Alanina Transaminase/sangue
Compostos de Aminobifenil/toxicidade
Animais
Animais Recém-Nascidos
Tetracloreto de Carbono/toxicidade
Dano ao DNA/efeitos dos fármacos
Dietilnitrosamina/toxicidade
Feminino
Heme Oxigenase-1/sangue
Interleucina-6/sangue
Masculino
Proteínas de Membrana/sangue
Camundongos
Camundongos Endogâmicos C57BL
NAD(P)H Desidrogenase (Quinona)/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Caracteres Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Carcinogens); 0 (Interleukin-6); 0 (Membrane Proteins); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (interleukin-6, mouse); 16054949HJ (4-biphenylamine); 3IQ78TTX1A (Diethylnitrosamine); CL2T97X0V0 (Carbon Tetrachloride); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); EC 1.6.5.2 (NAD(P)H Dehydrogenase (Quinone)); EC 1.6.5.2 (Nqo1 protein, mouse); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170508
[Lr] Data última revisão:
170508
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE


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[PMID]:26141568
[Au] Autor:Pery E; Sheehy A; Miranda Nebane N; Misra V; Mankowski MK; Rasmussen L; Lucile White E; Ptak RG; Gabuzda D
[Ad] Endereço:Department of Cancer Immunology and AIDS, Dana Farber Cancer Institute, Boston, MA 02115, United States; Department of Pathology, Harvard Medical School, Boston, MA 02115, United States.
[Ti] Título:Redoxal, an inhibitor of de novo pyrimidine biosynthesis, augments APOBEC3G antiviral activity against human immunodeficiency virus type 1.
[So] Source:Virology;484:276-87, 2015 Oct.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:APOBEC3G (A3G) is a cytidine deaminase that restricts HIV-1 replication by inducing G-to-A hypermutation in viral DNA; deamination-independent mechanisms are also implicated. HIV-1 Vif protein counteracts A3G by inducing its proteasomal degradation. Thus, the Vif-A3G axis is a potential therapeutic target. To identify compounds that inhibit Vif:A3G interaction, a 307,520 compound library was tested in a TR-FRET screen. Two identified compounds, redoxal and lomofungin, inhibited HIV-1 replication in peripheral blood mononuclear cells. Lomofungin activity was linked to A3G, but not pursued further due to cytotoxicity. Redoxal displayed A3G-dependent restriction, inhibiting viral replication by stabilizing A3G protein levels and increasing A3G in virions. A3G-independent activity was also detected. Treatment with uridine or orotate, intermediates of pyrimidine synthesis, diminished redoxal-induced stabilization of A3G and antiviral activity. These results identify redoxal as an inhibitor of HIV-1 replication and suggest its ability to inhibit pyrimidine biosynthesis suppresses viral replication by augmenting A3G antiviral activity.
[Mh] Termos MeSH primário: Compostos de Aminobifenil/metabolismo
Antivirais/metabolismo
Citidina Desaminase/metabolismo
HIV-1/imunologia
HIV-1/fisiologia
Pirimidinas/biossíntese
Replicação Viral
[Mh] Termos MeSH secundário: Desaminase APOBEC-3G
Células Cultivadas
Inibidores Enzimáticos/metabolismo
Seres Humanos
Leucócitos Mononucleares/virologia
Fenazinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Antiviral Agents); 0 (Enzyme Inhibitors); 0 (Phenazines); 0 (Pyrimidines); 26786-84-5 (lomofungin); 52962-95-5 (2,2'-((3,3'-dimethoxy(1,1'-biphenyl)-4,4'-diyl)diimino)bis-benzoic acid); EC 3.5.4.5 (APOBEC-3G Deaminase); EC 3.5.4.5 (APOBEC3G protein, human); EC 3.5.4.5 (Cytidine Deaminase); K8CXK5Q32L (pyrimidine)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150705
[St] Status:MEDLINE


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[PMID]:25922528
[Au] Autor:Wang S; Bott D; Tung A; Sugamori KS; Grant DM
[Ad] Endereço:Department of Pharmacology & Toxicology, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:Relative Contributions of CYP1A2 and CYP2E1 to the Bioactivation and Clearance of 4-Aminobiphenyl in Adult Mice.
[So] Source:Drug Metab Dispos;43(7):916-21, 2015 Jul.
[Is] ISSN:1521-009X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:4-Aminobiphenyl (ABP), a prototypical aromatic amine carcinogen in rodents and humans, requires bioactivation to manifest its toxic effects. A traditional model of ABP bioactivation, based on in vitro enzyme kinetic evidence, had postulated initial N-hydroxylation by the cytochrome P450 isoform CYP1A2. This is followed by phase 2 O-conjugation and hydrolysis to form a reactive nitrenium ion that covalently binds to DNA and produces tumor-initiating mutations. However, Cyp1a2(-/-) mice still possess significant liver ABP N-hydroxylation activity, DNA damage, and incidence of ABP-induced liver tumors, and in vivo induction of CYP1A2 paradoxically reduces levels of ABP-induced DNA damage. Competing ABP detoxification pathways can include N-acetylation by arylamine N-acetyltransferase 1 (NAT1) and/or NAT2; however, wild-type and Nat1/2(-/-) mice have similar in vivo ABP clearance rates. Together, these studies suggest the existence of novel ABP bioactivating and clearance/detoxification enzymes. In the present study, we detected similar reductions in Vmax for ABP N-hydroxylation by liver microsomes from Cyp1a2(-/-) and Cyp2e1(-/-) mice when compared with wild-type mice. In addition, recombinant mouse CYP1A2 and CYP2E1 were both able to N-hydroxylate ABP in mouse hepatoma cells. However, the in vivo clearance of ABP was significantly reduced in Cyp1a2(-/-) but not in Cyp2e1(-/-) mice. Our results support a significant role for CYP2E1 as a novel ABP N-oxidizing enzyme in adult mice, and suggest a more important contribution of CYP1A2 to the in vivo plasma clearance and thus detoxification of ABP.
[Mh] Termos MeSH primário: Compostos de Aminobifenil/metabolismo
Citocromo P-450 CYP1A2/genética
Citocromo P-450 CYP1A2/metabolismo
Citocromo P-450 CYP2E1/genética
Citocromo P-450 CYP2E1/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Ativação Metabólica/genética
Compostos de Aminobifenil/farmacocinética
Animais
Arilamina N-Acetiltransferase/genética
Arilamina N-Acetiltransferase/metabolismo
Linhagem Celular Tumoral
Dano ao DNA
Hidroxilação
Isoenzimas/genética
Isoenzimas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microssomos Hepáticos/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Isoenzymes); 16054949HJ (4-biphenylamine); EC 1.14.13.- (Cytochrome P-450 CYP2E1); EC 1.14.14.1 (Cytochrome P-450 CYP1A2); EC 2.3.1.5 (Arylamine N-Acetyltransferase); EC 2.3.1.5 (N-acetyltransferase 1); EC 2.3.1.5 (Nat2 enzyme, mouse)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150518
[Lr] Data última revisão:
150518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150430
[St] Status:MEDLINE
[do] DOI:10.1124/dmd.115.063297


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[PMID]:25601990
[Au] Autor:Wang S; Sugamori KS; Tung A; McPherson JP; Grant DM
[Ad] Endereço:*Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada M5S 1A8 and Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada M5S 3M2.
[Ti] Título:N-hydroxylation of 4-aminobiphenyl by CYP2E1 produces oxidative stress in a mouse model of chemically induced liver cancer.
[So] Source:Toxicol Sci;144(2):393-405, 2015 Apr.
[Is] ISSN:1096-0929
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:4-Aminobiphenyl (ABP) is a trace component of cigarette smoke and hair dyes, a suspected human carcinogen and a potent rodent liver carcinogen. Postnatal exposure of mice to ABP results in a higher incidence of liver tumors in males than in females, paralleling the sex difference in human liver cancer incidence. A traditional model of ABP tumorigenesis involves initial CYP1A2-mediated N-hydroxylation, which eventually leads to production of mutagenic ABP-DNA adducts that initiate tumor growth. However, several studies have found no correlation between sex or CYP1A2 function and the DNA-damaging, mutagenic, or tumorigenic effects of ABP. Oxidative stress may be an important etiological factor for liver cancer, and it has also been linked to ABP exposure. The goals of this study were to identify novel enzyme(s) that contribute to ABP N-oxidation, and to investigate a potential role for oxidative stress in ABP liver tumorigenicity. Isozyme-selective inhibition experiments using liver microsomes from wild-type and genetically modified mice identified CYP2E1 as a major ABP N-hydroxylating enzyme. The N-hydroxylation of ABP by transiently expressed CYP2E1 produced oxidative stress in cultured mouse hepatoma cells. In vivo postnatal exposure of mice to a tumorigenic dose of ABP also produced oxidative stress in male wild-type mice, but not in male Cyp2e1(-/-) mice or in female mice. However, a stronger NRF2-associated antioxidant response was observed in females. Our results identify CYP2E1 as a novel ABP-N-oxidizing enzyme, and suggest that sex differences in CYP2E1-dependent oxidative stress and antioxidant responses to ABP may contribute to the observed sex difference in tumor incidence.
[Mh] Termos MeSH primário: Compostos de Aminobifenil/farmacologia
Citocromo P-450 CYP2E1/metabolismo
Modelos Animais de Doenças
Neoplasias Hepáticas Experimentais/metabolismo
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Carcinógenos/toxicidade
Linhagem Celular Tumoral
Feminino
Hidroxilação
Neoplasias Hepáticas Experimentais/induzido quimicamente
Masculino
Camundongos
Microssomos Hepáticos/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Carcinogens); 16054949HJ (4-biphenylamine); EC 1.14.13.- (Cytochrome P-450 CYP2E1)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150121
[St] Status:MEDLINE
[do] DOI:10.1093/toxsci/kfv006


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[PMID]:25596734
[Au] Autor:Bhattacharya A; Klaene JJ; Li Y; Paonessa JD; Stablewski AB; Vouros P; Zhang Y
[Ad] Endereço:Department of Chemoprevention, Roswell Park Cancer Institute, Buffalo, NY, USA.
[Ti] Título:The inverse relationship between bladder and liver in 4-aminobiphenyl-induced DNA damage.
[So] Source:Oncotarget;6(2):836-45, 2015 Jan 20.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bladder cancer risk is significantly higher in men than in women. 4-Aminobiphenyl (ABP) is a major human bladder carcinogen from tobacco smoke and other sources. In mice, male bladder is more susceptible to ABP-induced carcinogenesis than female bladder, but ABP is more carcinogenic in the livers of female mice than of male mice. Here, we show that castration causes male mice to acquire female phenotype regarding susceptibility of bladder and liver to ABP. However, spaying has little impact on organ susceptibility to ABP. Liver UDP-glucuronosyltransferases (UGTs) are believed to protect liver against but sensitize bladder to ABP, as glucuronidation of ABP and its metabolites generally reduces their toxicity and promotes their elimination via urine, but the metabolites are labile in urine, delivering carcinogenic species to the bladder. Indeed, liver expression of ABP-metabolizing human UGT1A3 transgene in mice increases bladder susceptibility to ABP. However, ABP-specific liver UGT activity is significantly higher in wild-type female mice than in their male counterparts, and castration also significantly increases ABP-specific UGT activity in the liver. Taken together, our data suggest that androgen increases bladder susceptibility to ABP via liver, likely by modulating an ABP-metabolizing liver enzyme, but exclude UGT as an important mediator.
[Mh] Termos MeSH primário: Compostos de Aminobifenil/toxicidade
Dano ao DNA
Fígado/efeitos dos fármacos
Neoplasias da Bexiga Urinária/induzido quimicamente
Neoplasias da Bexiga Urinária/genética
Bexiga Urinária/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Masculino
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 16054949HJ (4-biphenylamine)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150119
[St] Status:MEDLINE


  10 / 613 MEDLINE  
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[PMID]:25224404
[Au] Autor:Juricek L; Bui LC; Busi F; Pierre S; Guyot E; Lamouri A; Dupret JM; Barouki R; Coumoul X; Rodrigues-Lima F
[Ad] Endereço:INSERM UMR-S 1124, Toxicologie Pharmacologie et Signalisation cellulaire, 45 rue des Saints-Pères, 75006, Paris, France.
[Ti] Título:Activation of the aryl hydrocarbon receptor by carcinogenic aromatic amines and modulatory effects of their N-acetylated metabolites.
[So] Source:Arch Toxicol;89(12):2403-12, 2015 Dec.
[Is] ISSN:1432-0738
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Aromatic amines (AAs) are an important class of chemicals which account for 12 % of known carcinogens. The biological effects of AAs depend mainly on their biotransformation into reactive metabolites or into N-acetylated metabolites which are generally considered as less toxic. Although the activation of the aryl hydrocarbon receptor (AhR) pathway by certain carcinogenic AAs has been reported, the effects of their N-acetylated metabolites on the AhR have not been addressed. Here, we investigated whether carcinogenic AAs and their N-acetylated metabolites may activate/modulate the AhR pathway in the absence and/or the presence of a bona fide AhR ligand (benzo[a]pyrene/B(a)P]. In agreement with previous studies, we found that certain AAs activated the AhR in human liver and lung cells as assessed by an increase in cytochrome P450 1A1 (CYP1A1) expression and activity. Altogether, we report for the first time that these properties can be modulated by the N-acetylation status of the AA. Whereas 2-naphthylamine significantly activated the AhR and induced CYP1A1 expression, its N-acetylated metabolite was less efficient. In contrast, the N-acetylated metabolite of 2-aminofluorene was able to significantly activate AhR, whereas the parent AA, 2-aminofluorene, did not. In the presence of B(a)P, activation of AhR or antagonist effects were observed depending on the AA or its N-acetylated metabolite. Activation and/or modulation of the AhR pathway by AAs and their N-acetylated metabolites may represent a novel mechanism contributing to the toxicological effects of AAs. More broadly, our data suggest biological interactions between AAs and other classes of xenobiotics through the AhR pathway.
[Mh] Termos MeSH primário: Carcinógenos/toxicidade
Citocromo P-450 CYP1A1/genética
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Receptores de Hidrocarboneto Arílico/efeitos dos fármacos
[Mh] Termos MeSH secundário: 2-Naftilamina/administração & dosagem
2-Naftilamina/metabolismo
2-Naftilamina/toxicidade
Acetilação
Compostos de Aminobifenil/administração & dosagem
Compostos de Aminobifenil/metabolismo
Compostos de Aminobifenil/toxicidade
Benzo(a)pireno/administração & dosagem
Benzo(a)pireno/farmacologia
Carcinógenos/metabolismo
Linhagem Celular
Citocromo P-450 CYP1A1/metabolismo
Fluorenos/administração & dosagem
Fluorenos/metabolismo
Fluorenos/toxicidade
Células Hep G2
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Receptores de Hidrocarboneto Arílico/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aminobiphenyl Compounds); 0 (Carcinogens); 0 (Fluorenes); 0 (Receptors, Aryl Hydrocarbon); 16054949HJ (4-biphenylamine); 3417WMA06D (Benzo(a)pyrene); 3A69OS195N (2-aminofluorene); CKR7XL41N4 (2-Naphthylamine); EC 1.14.14.1 (CYP1A1 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151209
[Lr] Data última revisão:
151209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140917
[St] Status:MEDLINE
[do] DOI:10.1007/s00204-014-1367-7



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