Base de dados : LILACS
Pesquisa : D08.244.453.491.375 [Categoria DeCS]
Referências encontradas : 9 [refinar]
Mostrando: 1 .. 9   no formato [Detalhado]

página 1 de 1

  1 / 9 LILACS  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1089317
Autor: Santos, Eliana Abreu; Gonçalves, José Carlos Saraiva; Fleury, Marcos K; Kritski, Afrânio L; Oliveira, Martha M; Velasque, Luciane S; Silva, José Roberto Lapa e; Estrela, Rita de Cássia E.
Título: Relationship of anti-tuberculosis drug-induced liver injury and genetic polymorphisms in CYP2E1 and GST
Fonte: Braz. j. infect. dis;23(6):381-387, Nov.-Dec. 2019. tab, graf.
Idioma: en.
Resumo: ABSTRACT Setting: Treatment of tuberculosis (TB) can result in Drug-Induced Liver Injury (DILI) since hepatotoxic metabolites are formed during the biotransformation of isoniazid (INH).DILI can be related to the genetic profile of the patient. Single nucleotide polymorphisms in the CYP2E1 gene and GSTM1 and GSTT1 deletion polymorphisms have been associated with adverse events caused by INH. Objective: To characterize the genetic polymorphisms of CYP2E1, GSTT1 and GSTM1 in TB carriers. Design: This is an observational prospective cohort study of 45 patients undergoing treatment of TB. PCR-RFLP and multiplex-PCR were used. Results: The distribution of genotypic frequency in the promoter region (CYP2E1 gene) was: 98% wild genotype and 2% heterozygous. Intronic region: 78% wild genotype; 20% heterozygous and 2% homozygous variant. GST enzyme genes: 24% Null GSTM1 and 22% Null GSTT1. Patients with any variant allele of the CYP2E1 gene were grouped in the statistical analyses. Conclusion: Patients with the CYP2E1 variant genotype or Null GSTT1 showed higher risk of presenting DILI (p = 0.09; OR: 4.57; 95% CI: 0.75-27.6). Individuals with both genotypes had no increased risk compared to individuals with one genotype.
Descritores: Tuberculose Pulmonar/tratamento farmacológico
Predisposição Genética para Doença/genética
Doença Hepática Induzida por Substâncias e Drogas/genética
Antituberculosos/efeitos adversos
-Polimorfismo Genético
Tuberculose Pulmonar/enzimologia
Estudos Prospectivos
Citocromo P-450 CYP2E1
Sistema Enzimático do Citocromo P-450/genética
Doença Hepática Induzida por Substâncias e Drogas/enzimologia
Família 2 do Citocromo P450
Genótipo
Fígado/efeitos dos fármacos
Fígado/enzimologia
Antituberculosos/uso terapêutico
Limites: Humanos
Masculino
Feminino
Adolescente
Adulto
Pessoa de Meia-Idade
Idoso
Idoso de 80 Anos ou mais
Adulto Jovem
Tipo de Publ: Estudo Observacional
Responsável: BR1.1 - BIREME


  2 / 9 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Texto completo
Id: biblio-974392
Autor: Maimaitimin, Kuerbanjiang; Jiang, Zhihui; Aierken, Aili; Shayibuzhati, Mikeremu; Zhang, Xiaoying.
Título: Hepatoprotective effect of Alhagi sparsifolia against Alcoholic Liver injury in mice
Fonte: Braz. J. Pharm. Sci. (Online);54(3):e17732, 2018. tab, graf.
Idioma: en.
Resumo: Overconsumption of alcohol leads to alcoholic liver disease (ALD). Natural compounds have been investigated previously for their hepatoprotective activities against liver injury. This study investigated the protective effect of Alhagi sparsifolia on ALD. Alcohol was administered to mice for three consecutive days; either alone or in combination with Alhagi sparsifolia extract (150, 300, 600 mg/kg). Serum aspartate aminotransferase and alanine transaminase as biomarkers of liver injury, the content of malonaldehyde, hydrogen peroxide (H2O2) and glutathione which indicated the redox status of liver and the antioxidant enzyme activity of super oxide dismutase were detected, respectively. Moreover, the expression of protein cytochrome P450 2E1 (CYP2E1) the key enzyme of alcohol metabolism, and also tested by western blot experiment. Subsequently, the mRNA levels of inflammatory factors including TNF- α and TLR4 was determined real-time PCR. Results showed that Alhagi sparsifolia significantly alleviated alcohol-induced liver injury by reducing serum ALT and AST, inhibiting MDA and H2O2 content, increasing SOD, and GSH level in the liver (P< 0.05). In addition, the Alhagi sparsifolia treatment inhibited the expression of CYP2E1 (P< 0.05). The results suggest that Alhagi sparsifolia could be a promising natural substance for ameliorating acute alcohol-induced oxidative stress and hepatic injury
Descritores: Fabaceae/efeitos adversos
Hepatopatias Alcoólicas
-Extratos Vegetais/uso terapêutico
Estresse Oxidativo
Citocromo P-450 CYP2E1
Cirrose Hepática Alcoólica/tratamento farmacológico
Antioxidantes/farmacologia
Limites: Animais
Feminino
Ratos
Responsável: BR1.1 - BIREME


  3 / 9 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
Texto completo
Texto completo
Id: biblio-983966
Autor: Gaviria Calle, Marcela; Duque Jaramillo, Alejandra; Aranzazu, Mateo; Filippo, Diana di; Montoya, Melissa; Roldán, Ingrid; Palacio, Natalia; Jaramillo, Sergio; Restrepo, Juan Carlos; Hoyos, Sergio; Navas, María Cristina.
Título: Polimorfismos en los genes de la enzima alcohol deshidrogenasa (ADH1) y la citocromo P450 2E1 (CYP2E1) en pacientes con cirrosis y carcinoma hepatocelular / Polymorphisms in alcohol dehydrogenase (ADH1) and cytochrome p450 2E1 (CYP2E1) genes in patients with cirrhosis and/or hepatocellular carcinoma
Fonte: Biomédica (Bogotá);38(4):555-568, oct.-dic. 2018. tab, graf.
Idioma: es.
Resumo: Introducción. Uno de los principales factores de riesgo del carcinoma hepatocelular es el consumo crónico de alcohol. En estudios en diferentes poblaciones, se sugiere que las variantes genéticas de las enzimas que participan en el metabolismo del alcohol, como la alcohol deshidrogenasa (ADH) y la citocromo P450 (CYP2E1), estarían asociadas con riesgo de enfermedades hepáticas terminales. Objetivo. Identificar y caracterizar las variantes alélicas de los genes ADH1B, ADH1C y CYP2E1 en pacientes colombianos con diagnóstico de cirrosis y carcinoma hepatocelular. Materiales y métodos. Se incluyeron muestras de pacientes atendidos entre el 2005 y el 2007, y entre el 2014 y el 2016, en la unidad de hepatología de un hospital de Medellín. La genotipificación de las muestras se hizo mediante reacción en cadena de la polimerasa (Polymerase Chain Reaction, PCR) con análisis de los polimorfismos en la longitud de los fragmentos de restricción (Restriction Fragment Length Polymorphism, RFLP). Los resultados se compararon con los de dos grupos de control y con lo reportado en la base de datos del 1000 Genomes Project. Resultados. Se recolectaron 97 muestras de pacientes con diagnóstico de cirrosis y carcinoma hepatocelular. Los dos factores de riesgo más frecuentes fueron el consumo crónico de alcohol (18,6 %) y las colangiopatías (17,5 %). Los genotipos más frecuentes en la población de estudio fueron el ADH1B*1/1 (82 %), el ADH1C*1/1 (59 %) y el CYP2E1*C/C (84 %). Conclusiones. En este primer estudio de los polimorfismos en pacientes colombianos con diagnóstico de cirrosis y carcinoma hepatocelular, los genotipos más frecuentes fueron el ADH1B*1/1, el ADH1C*1/1 y el CYP2E1*C/C. No se observaron diferencias estadísticamente significativas en la frecuencia de los genotipos entre los casos y los controles. Se requieren estudios adicionales en población colombiana para evaluar el riesgo de la enfermedad hepática terminal por consumo crónico de alcohol y la asociación con los polimorfismos.

Introduction: One of the most important risk factors for hepatocellular carcinoma (HCC) is alcohol consumption: Studies in different populations suggest that the risk of liver disease could be associated with genetic variants of the enzymes involved in alcohol metabolism, such as alcohol dehydrogenase (ADH) and cytochrome P450 CYP2E1. Objective: To identify and characterize the allelic variants of ADH1B, ADH1C and CYP2E1 genes in Colombian patients with cirrhosis and/or HCC. Materials and methods: We included samples from patients attending the hepatology unit between 2005-2007 and 2014-2016 of a hospital in Medellin. Samples were genotyped using PCR-RFLP. We compared the results with two control groups and the 1000 Genomes Project database. Results: We collected 97 samples from patients with a diagnosis of cirrhosis and/or HCC. The two main risk factors were chronic alcohol consumption (18.6%) and cholangiopathies (17.5%). The most frequent genotypes in the study population were ADH1B*1/1 (82%), ADH1C*1/1 (59%), and CYP2E1*C/C (84%). Conclusions: This first study of polymorphisms in Colombian patients diagnosed with cirrhosis and/or HCC showed genotypes ADH1B*1/1, ADH1C*1/1 and CYP2E1*C/C as the most frequent. We found no significant differences in the genotype frequency between cases and controls. Further studies are necessary to explore the association between polymorphisms and the risk of end-stage liver disease from alcohol consumption.
Descritores: Álcool Desidrogenase
Citocromo P-450 CYP2E1
-Carcinoma Hepatocelular/etiologia
Alelos
Genótipo
Cirrose Hepática/etiologia
Responsável: CO42.1 - Biblioteca Nacional de Salud José Celestino Mutis


  4 / 9 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-829258
Autor: De León-Nava, Marco A; Álvarez-Delgado, Carolina; Donis-Maturano, Luis; Hernández-Ruiz, Joselin; Manjarrez-Reyna, Aaron N; Cruz-Avilés, Edgar; Leon-Cabrera, Sonia; Morales-Montor, Jorge; Fragoso, José M; Escobedo, Galileo.
Título: A non-hepatotropic parasite infection increases mortality in the acetaminophen-induced acute liver failure murine model: possible roles for IL-5 and IL-6
Fonte: Mem. Inst. Oswaldo Cruz;111(12):757-764, Dec. 2016. graf.
Idioma: en.
Projeto: Consejo Nacional de Ciencia y Tecnología; . CICESE.
Resumo: We evaluated the effects of a non-hepatotropic parasite infection (Taenia crassiceps) on the outcome of acetaminophen-induced acute liver failure in mice. Uninfected and T. crassiceps infected mice orally received either 300 mg/kg acetaminophen or water as vehicle (n = 5 per group). Survival analysis, hepatocyte necrosis, alanine aminotransferase (ALT) levels, CYP2E1 protein, interleukin (IL-) 5, and IL-6 were assessed for all groups. All infected mice died within 16 h after exposure to acetaminophen (Tc+APAP group), whereas only one-third of uninfected animals exposed to acetaminophen (APAP group) died. Uninfected (Control group) and infected (Tc group) mice that received the vehicle showed no liver damage. Tc+APAP mice exhibited massive liver necrosis characterised by marked balloning degeneration of hepatocytes and higher serum ALT compared to Control, Tc, and APAP animals. Liver tissue from Tc+APAP mice also displayed increased expression of CYP2E1 protein and higher mRNA and protein levels of IL-5 and IL-6 compared to the other groups. These findings suggest that non-hepatotropic parasite infections may increase mortality following acute liver failure by promoting hepatocyte necrosis via IL-5 and IL-6-dependent CYP2E1 overproduction. This study identifies new potential risk factors associated with severe acute liver failure in patients.
Descritores: Acetaminofen
Analgésicos não Narcóticos
Falência Hepática Aguda
Teníase/parasitologia
-Acetaminofen/administração & dosagem
Alanina Transaminase/sangue
Analgésicos não Narcóticos/administração & dosagem
Biomarcadores/sangue
Citocromo P-450 CYP2E1/biossíntese
Citocromo P-450 CYP2E1/sangue
Modelos Animais de Doenças
Hepatócitos/parasitologia
Hepatócitos/patologia
Interleucina-5/sangue
Interleucina-6/sangue
Falência Hepática Aguda/induzido quimicamente
Falência Hepática Aguda/mortalidade
Falência Hepática Aguda/parasitologia
Falência Hepática Aguda/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Teníase/patologia
Limites: Animais
Feminino
Responsável: BR1.1 - BIREME


  5 / 9 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: lil-797893
Autor: Da Costa, N Meireles; Visoni, SBC; Dos Santos, IL; Barja-Fidalgo, TC; Ribeiro-Pinto, LF.
Título: Maternal protein restriction during lactation modulated the expression and activity of rat offspring hepatic CYP1A1, CYP1A2, CYP2B1, CYP2B2, and CYP2E1 during development
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;49(11):e5238, 2016. graf.
Idioma: en.
Resumo: Early nutrition plays a long-term role in the predisposition to chronic diseases and influences the metabolism of several drugs. This may happen through cytochromes P450 (CYPs) regulation, which are the main enzymes responsible for the metabolism of xenobiotics. Here, we analyzed the effects of maternal protein restriction (MPR) on the expression and activity of hepatic offspring’s CYPs during 90 days after birth, using Wistar rats as a mammal model. Hepatic CYP1A1, CYP1A2, CYP2B1, CYP2B2 and CYP2E1 mRNA and protein expression, and associated catalytic activities (ECOD, EROD, MROD, BROD, PROD and PNPH) were evaluated in 15-, 30-, 60-, and 90-day-old offspring from dams fed with either a 0% protein (MPR groups) or a standard diet (C groups) during the 10 first days of lactation. Results showed that most CYP genes were induced in 60- and 90-day-old MPR offspring. The inductions detected in MPR60 and MPR90 were of 5.0- and 2.0-fold (CYP1A2), 3.7- and 2.0-fold (CYP2B2) and 9.8- and 5.8– fold (CYP2E1), respectively, and a 3.8-fold increase of CYP2B1 in MPR90. No major alterations were detected in CYP protein expression. The most relevant CYP catalytic activities’ alterations were observed in EROD, BROD and PNPH. Nevertheless, they did not follow the same pattern observed for mRNA expression, except for an induction of EROD in MPR90 (3.5-fold) and of PNPH in MPR60 (2.2-fold). Together, these results suggest that MPR during lactation was capable of altering the expression and activity of the hepatic CYP enzymes evaluated in the offspring along development.
Descritores: Sistema Enzimático do Citocromo P-450/metabolismo
Dieta com Restrição de Proteínas
Lactação/metabolismo
Fígado/enzimologia
-Hidrocarboneto de Aril Hidroxilases/metabolismo
Citocromo P-450 CYP1A1/metabolismo
Citocromo P-450 CYP1A2/metabolismo
Citocromo P-450 CYP2B1/metabolismo
Citocromo P-450 CYP2E1/metabolismo
Modelos Animais
Ratos Wistar
Esteroide Hidroxilases/metabolismo
Fatores de Tempo
Limites: Animais
Feminino
Ratos
Responsável: BR1.1 - BIREME


  6 / 9 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
Id: lil-781927
Autor: Gaviria C, Mónica Marcela; Correa Arango, Gonzalo; Navas N, María Cristina.
Título: Alcohol, cirrosis y predisposición genética / Alcohol, Cirrhosis, and Genetic Predisposition
Fonte: Rev. colomb. gastroenterol;31(1):27-35, ene.-mar. 2016. ilus, tab.
Idioma: es.
Resumo: La cirrosis hepática es la tercera causa de muerte alrededor del mundo que es atribuible al consumo de alcohol. Más del 80% de los consumidores crónicos de alcohol desarrollan esteatosis y entre el 20% al 40% presentan otras complicaciones como fibrosis, hepatitis alcohólica y cirrosis; sin embargo, no todos los individuos con consumo crónico de alcohol desarrollan cirrosis, en parte debido al componente genético de cada individuo. El grado de actividad de las enzimas que metabolizan el alcohol está influenciado por polimorfismos presentes en los genes que codifican para estas enzimas, y corresponde a uno de los factores determinantes para el desarrollo de una hepatopatía terminal en respuesta al consumo de alcohol. Entre las enzimas implicadas en el metabolismo del alcohol están la alcohol deshidrogenasa (ADH), el citocromo P450 2E1 (CYP2E1) y la acetaldehído deshidrogenasa (ALDH), de las cuales se ha reportado que la mayor actividad de ADH y CYP2E1 y la menor actividad de ALDH pueden conferir riesgo en algunas poblaciones por la acumulación de acetaldehído, el cual es tóxico para el organismo. Se realizó una revisión en la literatura de los principales aspectos del metabolismo del alcohol y polimorfismos (genotipos) de enzimas que intervienen en el metabolismo del alcohol como factor de riesgo. Esto se hizo mediante la búsqueda de material bibliográfico a través de la base de datos PubMed desde 1990 hasta el 2013 utilizando las palabras claves alcohol liver disease, ADH, ALDH, CYP2E1 y polymorphism.

Liver cirrhosis is the third most common cause of death attributable to alcohol consumption throughout the world. More than 80% of chronic drinkers develop steatosis, and 20% to 40% develop other complications such as fibrosis, alcoholic hepatitis and cirrhosis. However, not everyone who chronically consumes alcohol develops cirrhosis. This is partly because of the genetic component of each individual. The level of activity of the enzymes that metabolize alcohol is influenced by polymorphisms of the genes that coding for these enzymes. This is one of the determining factors in the development of terminal liver disease in response to alcohol consumption. Among the enzymes involved in alcohol metabolism are alcohol dehydrogenase (ADH), cytochrome P450 2E1 (CYP2E1) and acetaldehyde dehydrogenase (ALDH). It has been reported that higher levels of activity of ADH and CYP2E1 and lower levels of activity of ALDH may be risk factors in some populations for accumulation of acetaldehyde which is toxic for the organism. This literature review covers the most important aspects of alcohol metabolism including polymorphisms (genotypes) of enzymes involved in the metabolism of alcohol as a risk factor. A search through the PubMed database from 1990 to be held 2013 was conducted using the keywords alcoholic liver disease, ADH, ALDH, CYP2E1, and polymorphism.
Descritores: Aldeído-Desidrogenase Mitocondrial
Citocromo P-450 CYP2E1
Síndrome de Secreção Inadequada de HAD
Hepatopatias Alcoólicas
Polimorfismo Genético
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CO332 - Facultad de Medicina


  7 / 9 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: lil-605937
Autor: Zhang, Daoxiang; Xiang, Taihe; Peihan, Li; Bao, Lumin.
Título: Transgenic plants of Petunia hybrida harboring the CYP2E1 gene efficiently remove benzene and toluene pollutants and improve resistance to formaldehyde
Fonte: Genet. mol. biol;34(4):634-639, 2011. ilus, graf.
Idioma: en.
Resumo: The CYP2E1 protein belongs to the P450 enzymes family and plays an important role in the metabolism of small molecular and organic pollutants. In this study we generated CYP2E1 transgenic plants of Petunia using Agrobacterium rhizogenes K599. PCR analysis confirmed that the regenerated plants contained the CYP2E1 transgene and the rolB gene of the Ri plasmid. Southern blotting revealed the presence of multiple copies of CYP2E1 in the genome of transgenic plants. Fluorescent quantitative PCR revealed exogenous CYP2E1 gene expression in CYP2E1 transgenic plants at various levels, whereas no like expression was detected in either GUS transgenic plants or wild-types. The absorption of benzene and toluene by transgenic plants was analyzed through quantitative gas chromatography. Transgenic plants with high CYP2E1 expression showed a significant increase in absorption capacity of environmental benzene and toluene, compared to control GUS transgenic and wild type plants. Furthermore, these plants also presented obvious improved resistance to formaldehyde. This study, besides being the first to reveal that the CYP2E1 gene enhances plant resistance to formaldehyde, also furnishes a new method for reducing pollutants, such as benzene, toluene and formaldehyde, by using transgenic flowering horticultural plants.
Descritores: Citocromo P-450 CYP2E1
Petunia/genética
Plantas Geneticamente Modificadas
-Benzeno
Formaldeído
Reação em Cadeia da Polimerase
Tolueno
Responsável: BR1.1 - BIREME


  8 / 9 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Cabello, Pedro Hernán
Texto completo
Id: lil-445674
Autor: Coura, Renata dos Santos; Marques, Christiane de Fátima Silva; Koifman, Rosalina J; Koifman, Sergio; Cabello, Pedro Hernan; Hatagima, Ana.
Título: CYP1A1 and CYP2E1 polymorphism frequencies in a large Brazilian population
Fonte: Genet. mol. biol;30(1):1-5, 2007. tab.
Idioma: en.
Resumo: The enzymes encoded by the polymorphic genes CYP1A1 and CYP2E1 play an important role in the activation and inactivation of xenobiotics. These enzymes have been associated with xenobiotic-induced diseases, such as cancer, therapeutic failure and adverse effects of drugs. The aim of the present study was to determine the allelic and genotypic frequencies of these polymorphisms in a large, ethnically mixed Brazilian population sample from Rio de Janeiro. Polymorphisms CYP1A1 and CYP2E1 were determined in 870 unrelated individuals by PCR-RFLP analysis in peripheral blood DNA. The observed allelic frequencies were 0.90 for CYP1A1*1A and 0.95 for CYP2E1*1A, in the total sample. The allelic frequency of CYP1A1*2C in "pardos" (0.13) and Brazilian whites (0.11) was higher than in Caucasians (0.05), which may be a result of the Amerindian genetic component, that presents the highest frequency of this allele observed up to now. The genotype distributions for both polymorphisms were in Hardy-Weinberg equilibrium and were statistically different between males and females, and among ethnic groups.
Descritores: Citocromo P-450 CYP1A1
Citocromo P-450 CYP2E1
Citocromos a1
Esteroide 17-alfa-Hidroxilase
Limites: Humanos
Masculino
Feminino
Responsável: BR1.1 - BIREME


  9 / 9 LILACS  
              first record previous record
seleciona
para imprimir
Fotocópia
Id: lil-333572
Autor: Azzalis, Ligia Ajaime.
Título: Interação de citocromo 2E1 induzido por etanol e estresse oxidativo / Interaction of cytochrome 2E1 ethanol-induced by and oxidative-stress.
Fonte: São Paulo; s.n; 2001. 100 p. tab, graf.
Idioma: pt.
Tese: Apresentada a Universidade de São Paulo. Instituto de Química para obtenção do grau de Doutor.
Resumo: Muitos autores associam as doenças alcoólicas às deficiências nutricionais. Por outro lado, trabalhos experimentais estabelecem que a hepatotoxicidade alcoólica relaciona-se especialmente à geração de espécies reativas através do sistema microsomal que oxida etanol via citocromo 450, principlamente o CYP2E1. O CYP2E1 hepático tem a capacidade de ativar algumas drogas comumente utilizadas, como o acetaminofeno, em seus metabólitos mais tóxicos e promover carcinogênese. Além disso, o metabolismo pelo CYP2E1 resulta num aumento na produção de espécies reativas, com diminuição nos sistemas de defesa antioxidantes, estabelecendo o estresse oxidativo. Como a expressão do CYP2E1 é muito influenciada...
Descritores: Citocromo P-450 CYP2E1
Espécies Reativas de Oxigênio/metabolismo
Etanol
Hepatopatias Alcoólicas/metabolismo
Estresse Oxidativo
-Western Blotting
Centrifugação
Coleta de Amostras Sanguíneas
Glutationa
Espectrofotômetros
Limites: Ratos
Responsável: BR40.1 - DBD - Divisão de Biblioteca e Documentacão do Conjunto das Químicas
BR40.1; 574.1921, A999i



página 1 de 1
   


Refinar a pesquisa
  Base de dados : Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde