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[PMID]: 26591610 [Au] Autor: Frolova TS; Sinitsyna OI; Kaledin VI [Ti] Título: [Mutagenic Activity of Four Aminoazo Compounds with Different Carcinogenicity for Rat Liver in the Ames Test]. [So] Source: Biofizika;60(5):990-4, 2015 Sep-Oct. [Is] ISSN: 0006-3029 [Cp] País de publicação: Russia (Federation) [La] Idioma: rus [Ab] Resumo: In this paper in the bacterial Ames test we compared the mutagenicity of four aminoazo compounds, previously studied by other researchers and used for activation of rat liver enzymes, with the carcinogenicity in the rat liver. It was found that in the Ames test they have mutagenic activity, however, this activity does not correlate quantitatively with rat sensitivity to their hepatocarcinogenic action. Thus, the most active carcinogen 3'-methyl-4-dimethylaminoazobenzene causes mutations almost 2.5 times less than weakly carcinogenic ortho-aminoazotoluene, and exactly the same number of mutations as non-carcinogenic N,N-diethyl-4-aminoazobenzene. [Mh] Termos MeSH primário: Compostos Azo/toxicidade Carcinógenos/toxicidade Mutagênicos/toxicidade Salmonella typhimurium/efeitos dos fármacos [Mh] Termos MeSH secundário: Animais Fígado/efeitos dos fármacos Fígado/patologia Metildimetilaminoazobenzeno/toxicidade Mutação/efeitos dos fármacos Ratos p-Aminoazobenzeno/análogos & derivados p-Aminoazobenzeno/toxicidade [Pt] Tipo de publicação: ENGLISH ABSTRACT; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Azo Compounds); 0 (Carcinogens); 0 (Mutagens); 2481-94-9 (C.I. Solvent Yellow 56); 55-80-1 (Methyldimethylaminoazobenzene); 57X2AH42T1 (p-Aminoazobenzene); F0U1H6UG5C (azobenzene) [Em] Mês de entrada: 1512 [Cu] Atualização por classe: 151120 [Lr] Data última revisão: 151120 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 151124 [St] Status: MEDLINE

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[PMID]: 25715596 [Au] Autor: Kaledin VI; Il'nitskaia SI; Ovchinnikova LP; Popova NA; Bogdanova LA; Morozkova TS [Ti] Título: [Mutagenic activation and carcinogenicity of aminoazo dyes of ortho-aminoazotoluene and 3'-methyl-4-dimethylaminoazobenzene in experiments on suckling mice]. [So] Source: Biofizika;59(3):527-32, 2014 May-Jun. [Is] ISSN: 0006-3029 [Cp] País de publicação: Russia (Federation) [La] Idioma: rus [Ab] Resumo: It is found that after administration of 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB,) which was hepatocarcinogenic to rats, in suckling mice, the number of neoplastic lesions in the liver of mice was 3 times higher than after analogous administration of equimolar dose of ortho-aminoazotoluene (OAT)). However, in the Ames test (TA-98 strain of Salmonella typhimurium) with activation by hepatic enzymes (S-9 fraction) of both intact and Aroclor-1254-induced mice and rats OAT contributed by an order of magnitude to revertant colonies compared to 3'-Me-DAB. In vivo inhibition of sulfotransferase activity, the enzyme which catalyzes the final stage of the mutagenic activation of aminoazo dyes, had no effect on carcinogenicity of 3'-Me-DAB but more than 4 times elevated that of OAT. It was concluded that the mechanism of carcinogenic action of aminoazo dyes studied is not genotoxic and that the carcinogenic potential of OAT is lost in the process of mutagenic activation. [Mh] Termos MeSH primário: Carcinógenos/toxicidade Corantes/toxicidade Neoplasias Hepáticas Experimentais Metildimetilaminoazobenzeno/toxicidade Mutagênicos/toxicidade o-Aminoazotolueno/toxicidade [Mh] Termos MeSH secundário: Animais Carcinógenos/farmacologia Corantes/farmacologia Fígado/enzimologia Fígado/patologia Neoplasias Hepáticas Experimentais/induzido quimicamente Neoplasias Hepáticas Experimentais/enzimologia Neoplasias Hepáticas Experimentais/genética Neoplasias Hepáticas Experimentais/patologia Metildimetilaminoazobenzeno/farmacologia Camundongos Camundongos Endogâmicos CBA Camundongos Endogâmicos ICR Mutagênicos/farmacologia Ratos Salmonella typhimurium/genética Salmonella typhimurium/metabolismo o-Aminoazotolueno/farmacologia [Pt] Tipo de publicação: ENGLISH ABSTRACT; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Carcinogens); 0 (Coloring Agents); 0 (Mutagens); 55-80-1 (Methyldimethylaminoazobenzene); QHZ900P7ZA (o-Aminoazotoluene) [Em] Mês de entrada: 1503 [Cu] Atualização por classe: 150226 [Lr] Data última revisão: 150226 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150227 [St] Status: MEDLINE

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[PMID]: 19596271 [Au] Autor: Hirano T; Sakai A; Ootsuyama Y; Kasai H [Ad] Endereço: Department of Life and Environment Engineering, Faculty of Environmental Engineering, The University of Kitakyushu, Kitakyushu, Fukuoka 808-0135, Japan. t-hirano@env.kitakyu-u.ac.jp [Ti] Título: Chronic alcohol consumption prevents 8-hydroxyguanine accumulation in 3'-methyl-4-dimethylaminoazobenzene-treated mouse liver. [So] Source: Biochem Biophys Res Commun;387(2):316-20, 2009 Sep 18. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Alcohol consumption is known to have opposing effects on carcinogenesis: promotion and prevention. In this study, we examined the effects of 12% ethanol on oxidative DNA damage accumulation and its repair in mouse livers treated with 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB), a well-known hepatic carcinogen. We previously reported that 3'-MeDAB increased 8-hydroxyguanine (8-OH-Gua) accumulation and its repair activity, accompanied by the fragmentation of 8-oxoguanine DNA glycosylase 1 (OGG1), the main repair enzyme of 8-OH-Gua. The present results showed that 12% ethanol intake attenuated the 8-OH-Gua accumulation, but not the fragmentation of OGG1 induced by 3'-MeDAB. Additionally, no significant changes in oxidative status, as monitored by lipid peroxidation (LPO), were observed among the 3'-MeDAB-treated mouse livers with/without alcohol administration. These findings suggested that 12% ethanol consumption may reduce the risk of 3'-MeDAB-induced carcinogenesis by decreasing 8-OH-Gua accumulation. [Mh] Termos MeSH primário: Consumo de Bebidas Alcoólicas/metabolismo Carcinógenos/toxicidade Transformação Celular Neoplásica/efeitos dos fármacos Etanol/administração & dosagem Guanina/análogos & derivados Fígado/efeitos dos fármacos Metildimetilaminoazobenzeno/toxicidade [Mh] Termos MeSH secundário: Consumo de Bebidas Alcoólicas/genética Animais Transformação Celular Neoplásica/induzido quimicamente Transformação Celular Neoplásica/metabolismo Dano ao DNA/efeitos dos fármacos Reparo do DNA/efeitos dos fármacos Guanina/metabolismo Fígado/metabolismo Masculino Camundongos Estresse Oxidativo/efeitos dos fármacos [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Carcinogens); 3K9958V90M (Ethanol); 55-80-1 (Methyldimethylaminoazobenzene); 5614-64-2 (8-hydroxyguanine); 5Z93L87A1R (Guanine) [Em] Mês de entrada: 0908 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 090715 [St] Status: MEDLINE [do] DOI: 10.1016/j.bbrc.2009.07.016

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[PMID]: 18683506 [Au] Autor: Bryzgalov LO; Ershov NI; Ilnitskaya SI [Ad] Endereço: Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Sciences, Novosibirsk. leon_l@ngs.ru [Ti] Título: FOXA transcription factors determine the amplitude of glucocorticoid induction of tyrosine aminotransferase in mice. [So] Source: Bull Exp Biol Med;144(5):722-4, 2007 Nov. [Is] ISSN: 0007-4888 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: o-Aminoazotoluene was more potent than 3'-methyl-4-dimethylaminoazobenzene in modulating glucocorticoid induction of tyrosine aminotransferase and DNA-binding activity of FOXA (HNF3) in 12-day-old ICR mice. In adult animals, induction of tyrosine aminotransferase and FOXA activity were modulated by o-aminoazotoluene, while 3'-methyl-4-dimethylaminoazobenzene was ineffective. Our results suggest that FOXA proteins determine glucocorticoid induction of tyrosine aminotransferase in mice (similarly to rats). [Mh] Termos MeSH primário: Fatores de Transcrição Forkhead/metabolismo Glucocorticoides/farmacologia Neoplasias Hepáticas/metabolismo Tirosina Transaminase/metabolismo [Mh] Termos MeSH secundário: Animais Ativação Enzimática/efeitos dos fármacos Fígado/efeitos dos fármacos Fígado/metabolismo Fígado/patologia Neoplasias Hepáticas/induzido quimicamente Metildimetilaminoazobenzeno Camundongos Camundongos Endogâmicos ICR Ligação Proteica/efeitos dos fármacos Fatores de Tempo o-Aminoazotolueno [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Forkhead Transcription Factors); 0 (Glucocorticoids); 55-80-1 (Methyldimethylaminoazobenzene); EC 2.6.1.5 (Tyrosine Transaminase); QHZ900P7ZA (o-Aminoazotoluene) [Em] Mês de entrada: 0812 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 080808 [St] Status: MEDLINE

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[PMID]: 18457031 [Au] Autor: Pakharukova MY; Smetanina MA; Kaledin VI; Kobzev VF; Romanova IV; Merkulova TI [Ad] Endereço: Institute of Cytology and Genetics, Siberian Division of Russian Academy of Sciences, Novosibirsk. pmaria@yandex.ru [Ti] Título: Activation of constitutive androstane receptor under the effect of hepatocarcinogenic aminoazo dyes in mouse and rat liver. [So] Source: Bull Exp Biol Med;144(3):338-41, 2007 Sep. [Is] ISSN: 0007-4888 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Selective increase of DNA-binding activity of constitutive androstane receptor was detected in rat and mouse liver in response to aminoazo dyes exhibiting hepatocarcinogenic activity for these species (ortho-aminoazotoluene for mice and 3'-methyl-4-dimethylaminobenzene for rats). Competition of azo dyes with 3H-5alpha-androst-16-ene-3alpha-ol (a well-known ligand of constitutive androstane receptor) for binding to liver cell cytosol proteins was studied. Ortho-aminoazotoluene and 3'-methyl-4-dimethylaminobenzene were better competitors for cytosol proteins from mouse and rat liver, respectively. [Mh] Termos MeSH primário: Corantes/metabolismo Metildimetilaminoazobenzeno/metabolismo Receptores Citoplasmáticos e Nucleares/metabolismo Fatores de Transcrição/metabolismo o-Aminoazotolueno/metabolismo [Mh] Termos MeSH secundário: Animais Seres Humanos Ligantes Neoplasias Hepáticas/induzido quimicamente Masculino Camundongos Ratos Ratos Wistar Receptores Citoplasmáticos e Nucleares/genética Fatores de Transcrição/genética [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Coloring Agents); 0 (Ligands); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Transcription Factors); 0 (constitutive androstane receptor); 55-80-1 (Methyldimethylaminoazobenzene); QHZ900P7ZA (o-Aminoazotoluene) [Em] Mês de entrada: 0806 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 080507 [St] Status: MEDLINE

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[PMID]: 17786350 [Au] Autor: Ando N; Shimizu M; Okuno M; Matsushima-Nishiwaki R; Tsurumi H; Tanaka T; Moriwaki H [Ad] Endereço: Department of Medicine, Gifu University School of Medicine, Gifu 501-1194, Japan. [Ti] Título: Expression of retinoid X receptor alpha is decreased in 3'-methyl-4-dimethylaminoazobenzene-induced hepatocellular carcinoma in rats. [So] Source: Oncol Rep;18(4):879-84, 2007 Oct. [Is] ISSN: 1021-335X [Cp] País de publicação: Greece [La] Idioma: eng [Ab] Resumo: The identification of the specific molecular targets, which underlie liver carcinogenesis is essential for the establishment of an effective strategy for the prevention and/or treatment of hepatocellular carcinomas (HCCs). We previously found that a malfunction of RXRalpha due to its aberrant phosphorylation was associated with the development of HCCs. However, it has remained unclear whether the abnormalities in the expression of RXRalpha or the other retinoid receptors play a role in the early stage of liver carcinogenesis. The present study was designed to determine whether alterations in the expression of RXRalpha and the other retinoid receptors RARalpha and RARbeta are involved in hepatocarcinogenesis using a 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB)-induced rat liver carcinogenesis model. We found that immunohistochemical expression of RXRalpha was decreased in liver cell tumors (HCCs and adenoma) and glutathione S-transferase placental form (GST-P)-positive foci, which is a precancerous lesion of HCC, when compared with the non-cancerous tissues. Western blot and RT-PCR analyses revealed a progressive decrease in the expression levels of RXRalpha, RARalpha, and RARbeta proteins and their mRNAs in 3'-MeDAB-induced HCCs and their surrounding tissues, when compared with the normal liver tissues from the control group. Moreover, the expression level of beta-catenin, the heterodimeric partner for both RXRalpha and RARalpha, was immunohistochemically observed in the cytoplasm and, in some cases, in the nucleus of HCC cells. The nuclear expression of cyclin D1, the downstream target molecule of beta-catenin, was also increased in HCC cells when compared with their adjacent normal appearing tissues. Our findings suggest that loss of retinoid receptors, especially RXRalpha, plays a critical role in the chemically-induced rat liver carcinogenesis and this might be associated with the activation of beta-catenin-related signaling pathway. [Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo Neoplasias Hepáticas Experimentais/metabolismo Metildimetilaminoazobenzeno/toxicidade Receptor X Retinoide alfa/metabolismo [Mh] Termos MeSH secundário: Adenoma/induzido quimicamente Adenoma/metabolismo Adenoma/patologia Animais Western Blotting Carcinoma Hepatocelular/induzido quimicamente Carcinoma Hepatocelular/patologia Núcleo Celular Ciclina D1/metabolismo Regulação Neoplásica da Expressão Gênica Glutationa S-Transferase pi/metabolismo Técnicas Imunoenzimáticas Neoplasias Hepáticas Experimentais/patologia Masculino RNA Mensageiro Ratos Ratos Endogâmicos F344 Receptores do Ácido Retinoico/metabolismo Receptor alfa de Ácido Retinoico Reação em Cadeia da Polimerase Via Transcriptase Reversa beta Catenina/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (RNA, Messenger); 0 (Rara protein, rat); 0 (Receptors, Retinoic Acid); 0 (Retinoic Acid Receptor alpha); 0 (Retinoid X Receptor alpha); 0 (beta Catenin); 0 (retinoic acid receptor beta); 136601-57-5 (Cyclin D1); 55-80-1 (Methyldimethylaminoazobenzene); EC 2.5.1.18 (Glutathione S-Transferase pi); EC 2.5.1.18 (Gstp1 protein, rat) [Em] Mês de entrada: 0711 [Cu] Atualização por classe: 161124 [Lr] Data última revisão: 161124 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 070906 [St] Status: MEDLINE

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[PMID]: 17626747 [Au] Autor: Chen QR; Xiang J; Liao B; Liu QB; Che LH; Xue L; Zhao GQ [Ad] Endereço: Department of Pathology, Zhongshan Medical School, Sun Yat-sen University, Guangzhou, Guangdong, 510080, P. R. China. [Ti] Título: [Evolutive characters of oval cells in experimental hepatocarcinogenesis]. [So] Source: Ai Zheng;26(7):719-23, 2007 Jul. [Cp] País de publicação: China [La] Idioma: chi [Ab] Resumo: BACKGROUND & OBJECTIVE: The role of oval cells in hepatocarcinogenesis is unclear yet. This study was to explore the correlation of oval cells to hepatocarcinoma through dynamic observation on evolutive characters of oval cells in experimental hepatocarcinogenesis. METHODS: Male SD rats were fed with 3o-me-DAB to establish an animal model of experimental hepatocarcinoma. Evolutive characters of oval cells in liver tissue during experimental hepatocarcinogenesis was dynamically observed with routine HE staining, Alcian blue staining, and immunohistochemistry. RESULTS: Oval cells (OV-6-positive) appeared sparsely around the portal tract in the 4th week of tumor-induction. In the 8th and the 14th weeks, OV-6-positive cells were increased gradually and expanded into hepatic lobules; the hepatic tissue was divided as pseudo-lobule-like. Till the 17th and the 24th weeks, carcinoma foci were formed, meanwhile, the total amount of oval cells were decreased, and OV-6-positive cells were observed in carcinoma foci. On Alcian blue-stained preparations, two distinct histologocal types of carcinoma foci could be seen: cholangioepithelial carcinoma foci were positive and hepatocellular carcinoma foci were negative. CONCLUSION: Oval cells, as intrahepatic stem cells, might play an important role in hepatocarcinogenesis. [Mh] Termos MeSH primário: Carcinoma Hepatocelular/patologia Colangiocarcinoma/patologia Hepatócitos/patologia Neoplasias Hepáticas Experimentais/patologia Células-Tronco/patologia [Mh] Termos MeSH secundário: Animais Carcinoma Hepatocelular/induzido quimicamente Colangiocarcinoma/induzido quimicamente Imuno-Histoquímica Fígado/patologia Neoplasias Hepáticas Experimentais/induzido quimicamente Masculino Metildimetilaminoazobenzeno Ratos Ratos Sprague-Dawley [Pt] Tipo de publicação: ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 55-80-1 (Methyldimethylaminoazobenzene) [Em] Mês de entrada: 0910 [Cu] Atualização por classe: 150313 [Lr] Data última revisão: 150313 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 070714 [St] Status: MEDLINE

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[PMID]: 17540316 [Au] Autor: Kelley FJ; Kopac CA; Rosselli J [Ad] Endereço: Family Nurse Practitioner Program, Georgetown University School of Nursing & Health Studies, Washington, DC 20057-1107, USA. kelleyj@georgetown.edu [Ti] Título: Advanced health assessment in nurse practitioner programs: follow-up study. [So] Source: J Prof Nurs;23(3):137-43, 2007 May-Jun. [Is] ISSN: 8755-7223 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The increase in advanced practice graduate programs and the inclusion of content and skills related to advanced health assessment as a core competency for practice served as the impetus for a 5-year follow-up study to track the changes, methodologies, and integration of technology into practitioner programs. The questionnaire was mailed to the faculty/schools listed as current members in the National Health Service Corps Nurse Practitioner Faculty Advocate Network. The number of responding schools was 135 (44%). The family nurse practitioner program continues to be the most offered advanced practice nursing program. Nearly all institutions offer a post-master's program and an advanced health assessment course to their clinical graduate students. Health assessment is usually taught concurrently or as a prerequisite for clinical experiences; there continues to be a strong emphasis on the physical examination component. Ethnic and cultural assessment and gerontological assessment content increased since the original study. Both class and laboratory class sizes decreased. Qualitative data that centered on differences in graduate versus undergraduate health assessment revealed a shift in focus in several areas: differential diagnoses, abnormals, and the inclusion of advanced skills. There was an emergence of more creative strategies: the use of standardized patients, online coursework, videotaping, "live" patients, and simulations. [Mh] Termos MeSH primário: Atitude do Pessoal de Saúde Bacharelado em Enfermagem/organização & administração Educação de Pós-Graduação em Enfermagem/organização & administração Profissionais de Enfermagem/educação Profissionais de Enfermagem/psicologia Avaliação em Enfermagem/organização & administração [Mh] Termos MeSH secundário: Distribuição de Qui-Quadrado Competência Clínica Currículo Diagnóstico Diferencial Seguimentos Seres Humanos Metildimetilaminoazobenzeno Profissionais de Enfermagem/organização & administração Papel do Profissional de Enfermagem/psicologia Pesquisa em Educação de Enfermagem Pesquisa Metodológica em Enfermagem Inovação Organizacional Exame Físico/enfermagem Autonomia Profissional Pesquisa Qualitativa Inquéritos e Questionários Ensino/organização & administração Estados Unidos [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 55-80-1 (Methyldimethylaminoazobenzene) [Em] Mês de entrada: 0708 [Cu] Atualização por classe: 151119 [Lr] Data última revisão: 151119 [Sb] Subgrupo de revista: IM; N [Da] Data de entrada para processamento: 070602 [St] Status: MEDLINE

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[PMID]: 16267830 [Au] Autor: Merkulova TI; Kropachev KY; Timofeeva OA; Vasiliev GV; Levashova ZB; Ilnitskaya SI; Kobzev VF; Pakharukova MY; Bryzgalov LO; Kaledin VI [Ad] Endereço: Laboratory of Gene Expression Control, Institute of Cytology and Genetics of the Siberian Division of Russian Academy of Sciences, Novosibirsk, Russia. [Ti] Título: Species-specific effects of the hepatocarcinogens 3'-methyl-4-dimethyl-aminoazobenzene and ortho-aminoazotoluene in mouse and rat liver. [So] Source: Mol Carcinog;44(4):223-32, 2005 Dec. [Is] ISSN: 0899-1987 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The effects of rat-specific hepatocarcinogen 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB), mouse-specific hepatocarcinogen ortho-aminoazotoluene (OAT), non-species-specific hepatocarcinogen diethylnitrosamine (DENA), and non-carcinogenic 4'-methyl-4-dimethylaminoazobenzene (4'-MeDAB) on glucocorticoid induction of tyrosine aminotransferase (TAT) and DNA-binding activity of hepatocyte nuclear factor 3 (HNF3) family of transcription factors were investigated with carcinogen-susceptible and -resistant animals. Species-specific hepatocarcinogens 3'-MeDAB and OAT strongly inhibited glucocorticoid induction of TAT in the liver of susceptible but not resistant animals. DENA, which is highly carcinogenic for the liver of both rats and mice inhibited glucocorticoid induction of TAT in both species, while non-carcinogenic 4'-MeDAB was absolutely ineffective both in rats and mice. The inhibition of TAT activity by the carcinogens was due to reduced levels of TAT mRNA, which is most likely to be a result of the reduced rate of transcription initiation of the TAT gene. In all cases, the TAT inhibition was accompanied by significant reduction of DNA-binding activity of the HNF3 transcription factor, which is known to be critical to glucocorticoid regulation of TAT gene. We also demonstrated that the described species-specific effects of OAT and of 3'-MeDAB on HNF3 DNA-binding activity may be initiated not only by administration in vivo, but also by their direct administration to homogenate, intact nuclei or nuclear lysate, but not to nuclear extract fraction, obtained by precipitation with 0.32 g/mL of ammonium sulfate (Fraction I). We showed, that a factor responsible for this effect might be precipitated in 0.32-0.47 g/mL interval of ammonium sulfate concentration. In contrast, non-specific hepatocarcinogen DENA was effective upon being added directly to Fraction I, implying a different mechanism of its action. [Mh] Termos MeSH primário: Carcinógenos/toxicidade Fator 3-alfa Nuclear de Hepatócito/biossíntese Neoplasias Hepáticas Experimentais/induzido quimicamente Fígado/efeitos dos fármacos Metildimetilaminoazobenzeno/toxicidade Tirosina Transaminase/biossíntese o-Aminoazotolueno/toxicidade [Mh] Termos MeSH secundário: Animais Núcleo Celular/metabolismo Dietilnitrosamina/toxicidade Indução Enzimática Glucocorticoides/farmacologia Fator 3-alfa Nuclear de Hepatócito/genética Fígado/metabolismo Neoplasias Hepáticas Experimentais/metabolismo Masculino Camundongos RNA Mensageiro/metabolismo Ratos Ratos Wistar Especificidade da Espécie Tirosina Transaminase/genética p-Dimetilaminoazobenzeno/toxicidade [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Carcinogens); 0 (Glucocorticoids); 0 (Hepatocyte Nuclear Factor 3-alpha); 0 (RNA, Messenger); 3IQ78TTX1A (Diethylnitrosamine); 55-80-1 (Methyldimethylaminoazobenzene); A49L8E13FD (p-Dimethylaminoazobenzene); EC 2.6.1.5 (Tyrosine Transaminase); QHZ900P7ZA (o-Aminoazotoluene) [Em] Mês de entrada: 0601 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 051104 [St] Status: MEDLINE

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[PMID]: 15860442 [Au] Autor: Sano T; Kagawa M; Okuno M; Ishibashi N; Hashimoto M; Yamamoto M; Suzuki R; Kohno H; Matsushima-Nishiwaki R; Takano Y; Tsurumi H; Kojima S; Friedman SL; Moriwaki H; Tanaka T [Ad] Endereço: Pharmaceutical Research Laboratories, Nikken Chemicals Co., Saitama, Japan. [Ti] Título: Prevention of rat hepatocarcinogenesis by acyclic retinoid is accompanied by reduction in emergence of both TGF-alpha-expressing oval-like cells and activated hepatic stellate cells. [So] Source: Nutr Cancer;51(2):197-206, 2005. [Is] ISSN: 0163-5581 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: We investigated the preventive effects of a synthetic acyclic retinoid, NIK-333, on the early and late events of hepatocarcinogenesis in male F344 rats treated with 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB). NIK-333 was administered once a day on consecutive days at a dose of 10, 40, or 80 mg/kg body weight along with the supplementation with 3'-MeDAB-containing diet for 16 wk. Animals from each group were sacrificed at 4 and 16 wk after the commencement of the experiment to determine the effect of NIK-333 on the early and late stages of carcinogenesis, respectively. NIK-333 suppressed the emergence of both oval-like cells expressing transforming growth factor (TGF)-alpha, putative progenitors of hepatocellular carcinoma (HCC), and activated hepatic stellate cells, major matrix-producing cells of the liver, in the early stage and inhibited the incidence of HCC in the late phase. These results suggest that NIK-333 is a promising drug for the chemoprevention of HCC by uniquely suppressing the early events of hepatocarcinogenesis, that is, development of both oval-like cells and fibrogenesis. [Mh] Termos MeSH primário: Actinas/metabolismo Adenoma/prevenção & controle Antineoplásicos/uso terapêutico Carcinoma/prevenção & controle Neoplasias Hepáticas Experimentais/prevenção & controle Fator de Crescimento Transformador alfa/metabolismo Tretinoína/análogos & derivados [Mh] Termos MeSH secundário: Actinas/efeitos dos fármacos Adenoma/induzido quimicamente Animais Antineoplásicos/química Carcinoma/induzido quimicamente Modelos Animais de Doenças Progressão da Doença Relação Dose-Resposta a Droga Fibrose/prevenção & controle Fígado/efeitos dos fármacos Fígado/metabolismo Neoplasias Hepáticas Experimentais/induzido quimicamente Masculino Metildimetilaminoazobenzeno/administração & dosagem Metildimetilaminoazobenzeno/análogos & derivados Ratos Ratos Endogâmicos F344 Retinoides/uso terapêutico Reação em Cadeia da Polimerase Via Transcriptase Reversa/métodos Fatores de Tempo Fator de Crescimento Transformador alfa/efeitos dos fármacos Tretinoína/química Tretinoína/uso terapêutico [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S. [Nm] Nome de substância: 0 (Actins); 0 (Antineoplastic Agents); 0 (Retinoids); 0 (Transforming Growth Factor alpha); 0 (smooth muscle actin, rat); 11ALM7A4RV ((2E,4E,6E,10E)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid); 3010-53-5 (3'-methyl-4-diethylaminoazobenzene); 55-80-1 (Methyldimethylaminoazobenzene); 5688UTC01R (Tretinoin); 81485-25-8 (3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid) [Em] Mês de entrada: 0510 [Cu] Atualização por classe: 141120 [Lr] Data última revisão: 141120 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 050430 [St] Status: MEDLINE

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