Base de dados : LILACS
Pesquisa : D08.244.453.484.250 [Categoria DeCS]
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Id: lil-684532
Autor: Brazilian Journal of Medical and Biological Research; Vasconcelos, R.B.; Salles, L.P.; Oliveira e Silva, I.; Gulart, L.V.M.; Souza, D.K.; Torres, F.A.G.; Bocca, A.L.; Rosa e Silva, A.A.M..
Título: Culture of bovine ovarian follicle wall sections maintained the highly estrogenic profile under basal and chemically defined conditions
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;46(8):700-707, ago. 2013. tab, graf.
Idioma: en.
Resumo: Follicle cultures reproduce in vitro the functional features observed in vivo. In a search for an ideal model, we cultured bovine antral follicle wall sections (FWS) in a serum-free defined medium (DM) known to induce 17β-estradiol (E2) production, and in a nondefined medium (NDM) containing serum. Follicles were sectioned and cultured in NDM or DM for 24 or 48 h. Morphological features were determined by light microscopy. Gene expression of steroidogenic enzymes and follicle-stimulating hormone (FSH) receptor were determined by RT-PCR; progesterone (P4) and E2 concentrations in the media were measured by radioimmunoassay. DM, but not NDM, maintained an FWS morphology in vitro that was similar to fresh tissue. DM also induced an increase in the expression of all steroidogenic enzymes, except FSH receptor, but NDM did not. In both DM and NDM, there was a gradual increase in P4 throughout the culture period; however, P4 concentration was significantly higher in NDM. In both media, E2 concentration was increased at 24 h, followed by a decrease at 48 h. The E2:P4 ratio was higher in DM than in NDM. These results suggest that DM maintains morphological structure, upregulates the expression of steroidogenic enzyme genes, and maintains steroid production with a high E2:P4 ratio in FWS cultures.
Descritores: Meios de Cultura/farmacologia
Estradiol/farmacologia
Folículo Ovariano/efeitos dos fármacos
Progesterona/farmacologia
Técnicas de Cultura de Tecidos
-Análise de Variância
Aromatase/genética
Meios de Cultura Livres de Soro
Enzima de Clivagem da Cadeia Lateral do Colesterol/genética
Expressão Gênica
Folículo Ovariano/anatomia & histologia
Fosfoproteínas/genética
Progesterona Redutase/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Receptores do FSH/genética
/genética
STEROID ABNORMALITIES, RADIATION-INDUCED-ALPHA-HYDROXYLASE/genética
Limites: Animais
Bovinos
Feminino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-633526
Autor: Pérez, María S.; Cerrone, Gloria E.; Benencia, Haydée; Márquez, Norma; De Piano, Eduardo; Frechtel, Gustavo D..
Título: Polimorfismos en los genes CYP11α y CYP17 y etiología del hiperandrogenismo en pacientes con poliquistosis ovárica / Polymorphism in CYP11alpha and CYP17 genes and the etiology of hyperandrogenism in patients with polycystic ovary syndrome
Fonte: Medicina (B.Aires);68(2):129-134, mar.-abr. 2008. ilus, tab.
Idioma: es.
Resumo: El síndrome de poliquistosis ovárica (PCOS) es un desorden endocrino-metabólico de naturaleza multifactorial, con una marcada predisposición genética, que afecta al 6% de las mujeres en edad reproductiva. Se caracteriza por la presencia de hiperandrogenismo, oligo-anovulación y ovarios poliquísticos. Entre los genes candidatos se encuentran aquellos que codifican para enzimas que actúan en la síntesis de andrógenos. Dos de los genes candidatos son el CYP17 y el CYP11alfa que codifican para la 17alfa hidroxilasa (P45017alfa) y para el P450scc (colesterol side chain cleavage) respectivamente. Los polimorfismos en estos genes están asociados al desarrollo del fenotipo hiperandrogénico. Nuestro objetivo fue analizar las frecuencias alélicas de los polimorfismos de los dos genes mencionados en población con PCOS, compararla con población normal y analizar la relación de cada variante alélica con el fenotipo hiperandrogénico correspondiente. Se analizaron 65 pacientes y 58 controles sanos en los que se determinaron niveles de testosterona y frecuencia de polimorfismos en los genes mencionados. Se observó una diferencia estadísticamente significativa cuando se asoció el grupo de mayor nivel de androgenemia con la presencia del genotipo A2/A2 del gen CYP17, y se hallaron mayores niveles de andrógenos circulantes en las pacientes con PCOS portadoras del alelo 216- del gen CYP11alfa. Nuestros resultados sugieren que ambos alelos juegan un rol menor en el desarrollo de PCOS y podrían ser considerados como potenciales marcadores de riesgo genético para el desarrollo del fenotipo hiperandrogénico.

The polycystic ovary syndrome (PCOS) is a heterogeneous multifactorial endocrine metabolic disorder with genetic predisposition affecting 6% of women in the reproductive age. This syndrome is characterized by the presence of oligo-anovulation, hyperandrogenism and polycystic ovaries. Several genes have been postulated as responsible for the etiology of this disorder. Among these genes are those encoding the enzymes involved in the ovarian androgen biosynthesis. Two of the candidate genes are the CYP17 and the CYP11alpha, encoding the 17-alpha-hydroxylase (P45017alpha) and the cholesterol side chain cleavage (P450scc) respectively. The polymorphisms of these genes are linked to the development of an hyperandrogenic phenotype. The aim of this work was to analyze the allelic frequencies of such polymorphisms in a cohort of women with PCOS and to compare them with those of healthy women. Furthermore, the correlation between each allelic variant and the corresponding hyperandrogenic phenotype was also assessed. Therefore, 65 patients and 58 age matched healthy controls were analyzed. The serum levels of testosterone and the frequency of each polymorphism were determined. When the PCOS population was analyzed, a significant statistical difference was found when relating the group with the highest androgenemia level with the presence of A2/A2 genotype of CYP 17 gene, and a higher level of circulating androgen was found in PCO women carrying the 216- allele of CYP11alpha gene (that did not reach statistical significance). Our results suggest that both alleles play a minor role in the development of PCOS and could be a genetic risk marker of the hyperandrogenic phenotype.
Descritores: Enzima de Clivagem da Cadeia Lateral do Colesterol/genética
Hiperandrogenismo/genética
Síndrome do Ovário Policístico/genética
Polimorfismo Genético/genética
/genética
STEROID ABNORMALITIES, RADIATION-INDUCED-ALPHA-HYDROXYLASE/genética
-Androgênios/análise
Androgênios/farmacocinética
Disponibilidade Biológica
Estudos de Casos e Controles
Marcadores Genéticos/genética
Reação em Cadeia da Polimerase
Polimorfismo de Fragmento de Restrição
Testosterona/análise
Testosterona/farmacocinética
Limites: Feminino
Seres Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: AR1.2 - Instituto de Investigaciónes Epidemiológicas


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Id: lil-223051
Autor: Rodríguez Montero, María del Carmen; Méndez Stivalet, José Manuel; Reyes Moreno, Mayra.
Título: Vía alternativa para la síntesis del 3-etilencetal-androsta-3, 17-diona / Alternative pathway for the synthesis of 3-ethylencetal-androsta-3, 17 dione
Fonte: Rev. cuba. farm;31(3):206-8, sept.-dic. 1997. graf.
Idioma: es.
Resumo: Se reporta una vía alternativa para la síntesis del 3-etilencetal-androsta-3, 17-diona, el cual es un intermedio importante para la obtención de corticoides por construcción de la cadena lateral de 17-ceto esteroides. En nuestro caso, partiendo de la androsta-4-ene-3, 17-diona, se obtuvo el producto deseado en 3 pasos de síntesis con buenos rendimientos
Descritores: Androsterona/antagonistas & inibidores
Androsterona/síntese química
Enzima de Clivagem da Cadeia Lateral do Colesterol
Via Alternativa do Complemento
Responsável: CU1 - INFOMED - Centro Nacional de Información de Ciencias Médicas


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Meneghelli, U. G
Id: lil-148773
Autor: Martinelli, A. L; Meneghelli, U. G; Zucoloto, S.
Título: Cytochrome P450 and glutathione in the liver of rats under exclusive sucrose ingestion
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;26(9):989-98, Sept. 1993. tab.
Idioma: en.
Resumo: 1. The objective of the present investigation was to study some of the possible mechanisms involved in the protective effect of sucrose ingestion against liver necrosis induced by acetaminophen. Three groups of male Wistar rats (220-260 g) were submitted to the following experimental conditions for a period of 42 h: free access to a balanced commercial diet (Group I), an exclusive sucrose diet (Group II) and fasting (Group III). At the end of the experiment, hepatic cytochrome P450 levels were measured in 11 rats from each group, plasma antipyrine half-life (t1/2) was determined in 40 rats from each group, and hepatic glutathione (GSH) concentration in 10 rats from each group. GSH consumption elicited by a high dose of acetaminophen (ACP, 1.0 g/kg, by gavage) was also determined in 30 rats each from Groups II and III. 2. The liver of Group II rats presented a significant reduction of cytochrome P450 levels in the microsome fraction (range 0.31-0.46, median, 0.37 nmol/mg vs range 0.60-0.93, median 0.74 for group I, and range 0.63-1.22, median 0.91 for group III, reported as nmol/mg microsome protein; range 23.8-48.4, median 40.4 vs 66.6-130, median 81.8 for group I and range 59.0-117.1, median 77.1 for group III, reported as nmol/100 g body weight), and a prolongation of antipyrine half-life (146.4 vs 83.4 min for group I and 93.6 for group III) when compared with the rats of the two other groups. 3. Since the toxicity of acetaminophen depends on the production of a reactive metabolite by the cytochrome P450 system in the liver, we conclude that changes in this system brought about by exclusive sucrose ingestion for 42 h may explain the liver protection against the toxicity of a high dose of the drug even in the presence of a significant concomitant reduction in liver GSH levels
Descritores: Acetaminofen/toxicidade
Enzima de Clivagem da Cadeia Lateral do Colesterol/metabolismo
Fígado
Glutationa/metabolismo
Sacarose/administração & dosagem
-Antipirina/sangue
Peso Corporal
Jejum
Fígado/metabolismo
Fígado/patologia
Microssomos Hepáticos
Microssomos Hepáticos/metabolismo
Necrose
Ratos Wistar
Fatores de Tempo
Limites: Animais
Masculino
Ratos
Tipo de Publ: Estudo Comparativo
Responsável: BR1.1 - BIREME


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Id: lil-138030
Autor: Cattani O., Andreína.
Título: Hiperplasia suprarrenal congénita: formas de presentación clínica y evaluación diagnóstica / Congenital adrenal hyperplasia: clinical presentation forms and diagnosis evaluation
Fonte: Rev. chil. pediatr;64(1,supl):49-54, 1993. tab.
Idioma: es.
Descritores: Hiperplasia Suprarrenal Congênita/genética
-3-Hidroxiesteroide Desidrogenases/deficiência
Enzima de Clivagem da Cadeia Lateral do Colesterol/deficiência
Hiperplasia Suprarrenal Congênita/complicações
Hiperplasia Suprarrenal Congênita/fisiopatologia
Esteroide 11-beta-Hidroxilase/deficiência
Esteroide 17-alfa-Hidroxilase/deficiência
Esteroide 21-Hidroxilase/deficiência
Limites: Recém-Nascido
Lactente
Pré-Escolar
Criança
Responsável: CL1.1 - Biblioteca Central



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