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1.
J. physiol. biochem ; 73(1): 37-48, feb. 2017. ilus, tab, graf
Artigo em Inglês | IBECS | ID: ibc-168391

RESUMO

The effect of exercise-induced oxidative stress on health and aging is not clearly explained. This study examined the effects of habitual sport practice, age, and submaximal exercise on the blood markers of oxidative stress, muscle damage, and antioxidant response. Seventy-two healthy men were grouped by their habitual sport practice: inactive (<1.5 h/week), recreational (3-8 h/week), and trained athletes (>8 h/week), and further divided by age: young (18-25 years), adult (40-55 years), and senior (>55 years). Blood samples were collected at rest and after submaximal effort. Hydroperoxides and superoxide dismutase, glutathione peroxidase, and catalase activities were measured by spectrophotometry. Nuclear DNA damage was analyzed by comet assay. The alpha-actin release was analyzed by Western blot. Alpha-tocopherol, retinol, and coenzyme-Q10 were quantified by high-performance liquid chromatography analysis. Data was analyzed through a factorial ANOVA and the Bonferroni post hoc test. Lipid peroxidation increased significantly with age and submaximal effort (p < 0.05). However, the trained athlete group presented lower lipid peroxidation compared with the recreational group (MD = 2.079, SED = 0.58, p = 0.002) and inactive group (MD = 1.979, SED = 0.61, p = 0.005). Trained athletes showed significant higher alpha-actin levels (p < 0.001) than the other groups. Recreational group showed lower nuclear DNA damage than trained athletes (MD = 3.681, SED = 1.28, p = 0.015). Nevertheless, the inactive group presented significantly higher superoxide dismutase and catalase (p < 0.05) than the other groups. Data suggested that habitual competitive training practice could prevent age-related increases of plasma lipid peroxidation, which, according with our results, cannot be entirely attributed to blood antioxidant defense systems (AU)


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Assuntos
Humanos , Masculino , Adolescente , Adulto Jovem , Adulto , Pessoa de Meia-Idade , Envelhecimento/etnologia , Comportamento Competitivo , Exercício Físico , Peroxidação de Lipídeos , Músculo Esquelético/fisiologia , Estresse Oxidativo , Dano ao DNA , Atletas , Biomarcadores/sangue , Esportes , Espanha , Comportamento Sedentário , Recreação , Ensaio Cometa
2.
Rev. toxicol ; 32(2): 121-126, 2015. tab, graf
Artigo em Espanhol | IBECS | ID: ibc-146473

RESUMO

La exposición a partículas ambientales es un factor de riesgo que ocasiona daños en la salud humana, como trastornos respiratorios, cardiovasculares y cáncer. La toxicidad y el efecto inflamatorio de estas partículas están relacionados con su tamaño y características químicas. El objetivo de este estudio fue determinar las características químicas de la fracción hidrosoluble de Material Particulado PM10, recolectado en tres sitios de monitoreo de la ciudad de Cuenca-Ecuador, y evaluar su actividad genotóxica e inducción de especies reactivas de oxígeno (ROS) en la línea celular epitelial alveolar humana A-549. Las muestras fueron recolectadas empleando un equipo de bajo volumen. Las concentraciones de material particulado determinadas por análisis gravimétrico superaron en los tres puntos de estudio los 50 µg/m3, límite estipulado en la Legislación Ecuatoriana. En la caracterización de la solución acuosa se determinó la presencia de aniones (Cl-, NO3-, SO4-2) y metales pesados (Cr, Fe, Ni, Zn, Cu, Mn), mediante técnicas de cromatografía iónica y espectroscopía de absorción atómica respectivamente; SO4-2 y Fe presentaron las mayores concentraciones. Las células A-549 fueron expuestas a diferentes concentraciones (0,82; 1,25 y 1,63 m3/mL) de la fracción hidrosoluble de PM10, con la finalidad de observar el posible efecto genotóxico mediante el ensayo del cometa y la inducción de especies reactivas de oxígeno mediante fluorimetría. Finalmente se determinó que los extractos acuosolubles de PM10 inducen daño celular bajo (tipo I), e incrementan la producción de ROS en células A-549, lo que pudiera constituir un riesgo en la salud de la población expuesta (AU)


Exposure to environmental particles is a risk factor that causes damage to human health, such as respiratory and cardiovascular diseases and cancer. The toxicity and inflammatory effects of these particles is related to their size and chemical characteristics . The aim of this study was to determine the chemical characteristics of the aqueous fraction of Particulate Matter PM 10, collected in three monitoring sites Cuenca-Ecuador, a nd to evaluate their genotoxic activity and induction of reactive oxygen species (ROS) in human alveolar epithelial cell line A-549. Samples were collected using a low volume equipment. Particulate matter concentrations determined by gravimetric analysis in the three study points exceeded the 50ug/m3 limit stated in the Ecuadorian legislation. In the characterization of the aqueous solution the presence of anions (Cl-, NO3-, SO4-2) and heavy metals (Cr, Fe, Ni, Zn, Cu, Mn) was determined by ion chromatography techniques and atomic absorption spectroscopy, respectively; SO4-2 and Fe showed the highest concentrations. The A-549 cells were exposed to different concentrations (0.82, 1.25 and 1.63 m3 / mL) fraction of water-soluble PM10, in order to observe the possible genotoxic effect by the comet assay and the amount inducing reactive oxygen species by fluorimetry. It was finally determined that the aqueous -soluble extracts of PM10 induce cell damage under (type I), and increase the production of ROS in cells A-549, which could pose a risk to the health of the exposed population of the city of Cuenca (AU)


Assuntos
Testes de Mutagenicidade/métodos , Testes de Mutagenicidade/normas , Genotoxicidade/análise , Genotoxicidade/métodos , Estresse Oxidativo , Células Epiteliais/classificação , Células Epiteliais/patologia , Fatores de Risco , Carcinógenos Ambientais/toxicidade , Poluentes Ambientais/efeitos adversos , Poluentes Ambientais/toxicidade , Poluição do Ar/efeitos adversos , Ensaio Cometa/métodos , Ensaio Cometa
3.
J. physiol. biochem ; 70(4): 981-990, dic. 2014. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-131431

RESUMO

Lycopene is a carotenoid pigment produced by vegetables and fruits, with tomatoes and their processed products being the most abundant sources. A high number of conjugated dienes make lycopene a powerful radical scavenger. Its antioxidant properties are considered to be primarily involved in many beneficial health effects. The present study was designed to assess the protective effect of lycopene-enriched tomato paste against N-nitrosodiethylamine (NDEA)-induced oxidative stress in rats. Forty-eight male Wistar rats were divided randomly into six groups. Four groups were treated with tomato paste, per os, for 28 days in doses which were equivalent to 0.5 (groups II and V) and 2.5 mg/kg b.w./day of lycopene (groups III and VI). Rats from groups IV-VI were given intraperitoneally a single dose of NDEA, 150 mg/kg b.w. Group I (control) was given distilled water. Pretreatment with tomato paste protected the antioxidant enzymes: superoxide dismutase, catalase and glutathione reductase. Their activity was recovered by 32-97 %, as compared to NDEA-treated rats. Microsomal lipid peroxidation in the liver was decreased in rats pretreated with a lower dose of tomato paste by 28 %, as compared to animals given NDEA alone. Pretreatment with tomato paste caused a decrease in plasma concentration of protein carbonyls, even below the control level, in rats given NDEA. Moreover, a 10 % reduction of DNA damage in leucocytes caused by NDEA was observed. The tomato paste tested was able to suppress NDEA-induced oxidative stress in rats (AU)


Assuntos
Animais , Ratos , Antioxidantes/farmacocinética , Concentrados de Tomates , Estresse Oxidativo , Modelos Animais de Doenças , Substâncias Protetoras/farmacocinética , Peroxidação de Lipídeos , Ensaio Cometa/métodos , Carbonilação Proteica
4.
Av. odontoestomatol ; 30(1): 29-38, ene.-feb. 2014. ilus
Artigo em Espanhol | IBECS | ID: ibc-120682

RESUMO

Objetivo: Analizar la evidencia científica disponible acerca de la genotoxicidad causada por los monómeros dentales liberados de las resinas compuestas. Materiales y métodos: Se lleva a cabo una búsqueda electrónica exhaustiva de estudios relacionados con la genotoxicidad de las resinas compuestas o los monómeros dentales utilizando las bases de datos Pubmed, OvidSP, EbscoHost, SciVerse y SpringerLink. Se revisaron un total de 115 artículos y se seleccionaron 36 entre estudios clínicos controlados, estudios en animales y pruebas in vitro. Conclusiones: La exposición a los monómeros residuales liberados por las resinas compuestas, causa gran preocupación por los estudios que advierten su potencial genotóxico. El principal mecanismo es atribuido al estrés oxidativo que se genera por aumento de las concentraciones de radicales libres y disminución de los niveles de glutatión, agente responsable del balance redox en la célula. Estas alteraciones conllevan a la activación de varias vías de apoptosis celular y retrasos en las fases G1 y G2 del ciclo celular (AU)


Objective: To examine the available scientific evidence about the genotoxicity caused by monomers released from dental composite resins. Materials and methods: We carried out a comprehensive electronic search of studies related to the genotoxicity of composite resins or dental monomers using the databases PubMed, OvidSP, EBSCOhost, and SciVerseSpringerLink. We reviewed a total of 115 articles and 36 were selected from controlled clinical studies, animal studies and in vitro tests. Conclusions: Exposure to residual monomers released from composites, causes great concern about studies that warn their genotoxic potential. The main mechanism is attributed to oxidative stress is generated by increasing concentrations of free radicals and decreased levels of Glutathione redox agent responsible for the cell balance. These changes lead to the activation of multiple pathways of apoptosis and delays in G1 and G2 phases of the cell cycle (AU)


Assuntos
Humanos , Genotoxicidade/análise , Resinas Compostas/efeitos adversos , Dano ao DNA , Testes de Mutagenicidade/métodos , Micronúcleos com Defeito Cromossômico , Ensaio Cometa/métodos , Estresse Oxidativo
5.
Nutr. hosp ; 25(1): 39-48, ene.-feb. 2010. ilus, tab
Artigo em Inglês | IBECS | ID: ibc-80804

RESUMO

Etoricoxib, a second generation selective cyclooxygenase-2 (COX-2) inhibitor had been studied for the chemopreventive response at its therapeutic anti-inflammatory dose in 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis in rat model. Eight to ten weeks old male rats of Sprague-Dawley strain were divided into four groups. While group 1 served as control and received the vehicle of the drugs, group 2 and 3 were administered freshly prepared DMH in 1mM EDTA-saline (pH 7.0) (30 mg/kg body wt/week, subcutaneously). Group 3 was also given a daily treatment of etoricoxib (0.6 mg/kg body wt orally) while the group 4 received the same amount of etoricoxib only, prepared in 0.5% carboxymethyl cellulose. Animals were sacrificed at the end of 6 weeks, body weight recorded and the colons were subjected to macroscopic and histopathological studies. The maximum number of raised mucosal lesions called the multiple plaque lesions (MPL) were found in the DMH group which significantly reverted back in the DMH + etoricoxib group, while very few MPLs were recorded in the control and etoricoxib only group. Similarly, the number of aberrant crypt foci (ACF), the point of future carcinogenic growth, was recorded more in the DMH group and significantly less in the DMH + etoricoxib group. The histopathological analysis showed the presence of severe hyperplasia, occasional dysplasia and aggregates of lymphoid cells in the localized regions. Etoricoxib group showed near normal histological features with the crypt architecture and the surrounding stromal tissue remaining intact. To ascertain the molecular mechanism of such anti-carcinogenic features the colonocytes were isolated and studied in primary culture for the evidence of apoptosis by fluorescent staining and genotoxic changes by single cell gel electrophoresis assay (comet assay) which shows that the DMH treated animals produced much less apoptotic nuclei but more comet producing cell, while these features were reverted back with the etoricoxib treatment. The cytoplasmic expression of COX-2 protein was studied in paraffin sections of the colon by immunohistochemistry with COX-2 specific antibody which showed a very high presence of this inducible enzyme with the DMH group while in all other groups of animals it was not visible or weekly expressed. The anti-inflammatory effect of the drug, etoricoxib was also validated by a carrageenan-induced inflammation in rat model which showed an extremely high anti-inflammatory response within the dose range used in the present study. Also the growth profile of all the animals remained the same throughout the six week period of the investigation as there was no change in the body weight. It appears that apoptosis remains the dominant anti-proliferative end effect of this drug, mediated by an inhibition of the proinflammatory COX-2 isoform although further molecular probings are needed to arrive at a conclusive agreement in favor of the chemoprotective use of such drugs in colon cancers (AU)


El Etoricoxib, un inhibidor selectivo de la ciclooxigenasa-2 (COX-2) de segunda generación, se ha estudiado por la respuesta quimiopreventiva a su dosis terapéutica antiinflamatoria en un modelo murino de carcinogénesis colónica inducida por 1,2-dimetilhidracina (DMH). Se dividió en cuatro grupos a ratas de la cepa Sprague-Dawley de ocho a diez semanas de vida. El grupo 1 sirvió de control y recibió el vehículo de los fármacos, y a los grupos 2 y 3 se les administró DMH recién preparada en EDTA-salino al 1 mM (pH 7,0) (30 mg/kg peso corporal/semana, subcutáneamente). El grupo 3 también recibió a diario tratamiento con etoricoxib (0,6 mg/kg peso corporal, por vía oral), mientras que el grupo 4 solamente recibió la misma cantidad de etoricoxib, preparado en 0,5% carboximetil celulosa. Se sacrificó a los animales al final de la sexta semana, se registró el peso corporal y se realizaron estudios macroscópicos e histopatológicos del colon. El número máximo de lesiones mucosas elevadas, denominadas lesiones en placa múltiples (LPM) se halló en el grupo DMH, y estaba significativamente normalizado en el grupo de DMH + etoricoxib, mientras que se hallaron muy pocas lesiones LPM en los grupos control y con sólo etoricoxib. De forma similar, el número de focos de criptas aberrantes (FCA), el punto del futuro crecimiento carcinogénico, se registró más abundantemente en el grupo DMH y menos significativamente en el grupo DMH + etoricoxib. El análisis histopatológico mostró la presencia de una hiperplasia marcada, displasia ocasional y agregados de células linfoides en las regiones localizadas. El grupo de etoricoxib mostró unas características histológicas casi normales, permaneciendo la arquitectura de las criptas y el tejido estromal vecino intacto. Para determinar el mecanismo molecular de tales hallazgos anticarcinogénicos, se aislaron los colonocitos y se estudiaron en un cultivo primario para evidencia de apoptosis mediante tinción fluorescente y cambios genotóxicos en un ensayo de electroforesis en gel de una única célula (ensayo comet), que mostró que los animales tratados con DMH produjeron muchos menos núcleos apoptóticos pero un mayor número de células productoras de comet, mientras que estos cambios revirtieron con el tratamiento con etoricoxib. Se estudió la expresión citoplásmica de la proteína COX-2 en las secciones en parafina del colon mediante inmunohistoquímica con un anticuerpo específico anti-COX-2 que mostró una presencia muy alta de esta enzima inducible en el grupo DMH mientras que en el resto de los grupos de animales apenas se expresó o no se visualizó. Efecto antiinflamatorio del fármaco: el etoricoxib también se validó en modelo murino de inflamación inducida por carragenina que mostró una respuesta antiinflamatoria extremadamente alta dentro del rango de dosis empleado en este estudio. El perfil de crecimiento de los animales permaneció inalterado durante las seis semanas que duró la investigación y no hubo cambios en el peso corporal. Parece que la apoptosis sigue siendo el efecto antiproliferativo final dominante de este fármaco mediado por la inhibición de la isoforma proinflamatoria de la COX-2, si bien se necesitan probandos moleculares adicionales para llegar a un acuerdo concluyente a favor del uso quimiopreventivo de tales fármacos en los cánceres de colon (AU)


Assuntos
Animais , Masculino , Ratos , 1,2-Dimetilidrazina , Carcinógenos , Apoptose , Colo/patologia , Inibidores de Ciclo-Oxigenase 2/uso terapêutico , Carragenina , Proliferação de Células , Colite/induzido quimicamente , Colite/prevenção & controle , Neoplasias do Colo/induzido quimicamente , Ensaio Cometa , Imuno-Histoquímica
6.
Rev. toxicol ; 21(2/3): 92-97, 2004. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-125985

RESUMO

La respuesta individual al daño en el ADN inducido por agentes xenobióticos está condicionada por la eficacia de los sistemas de reparación. Algunos de los polimorfismos genéticos descritos en las enzimas de reparación del ADN pueden afectar a su función, determinando una variación en la susceptibilidad ante la exposición a agentes ambientales. El objetivo de este estudio ha consistido en investigar si las variantes alélicas más frecuentes de las enzimas de reparación XRCC1 ( Arg194Trp y Arg399Gln ), XRCC3 ( Thr241Met ) o APE1 ( Asp148Glu ) pueden condicionar el daño en el ADN inducido por el estireno y su principal metabolito, el estireno-7,8-óxido (EO). Leucocitos periféricos de 30 voluntarios sanos se trataron con estireno o EO, y el daño en el ADN inducido se evaluó mediante el ensayo del cometa. Tras el tratamiento con estireno, los individuos portadores de los alelos XRCC1 399Gln y XRCC3 241Met mostraron mayor nivel de roturas en el ADN, sugiriendo menor eficacia de los sistemas de reparación. Por el contrario, los portadores del alelo APE1 148Glu mostraron daño en el ADN significativamente menor que los individuos 148 Asp/Asp . Sin embargo, no se obtuvo ningún efecto significativo en las células expuestas a EO, debido probablemente a que el daño inducido es inicialmente mayor, y no permite que se pongan de manifiesto pequeñas diferencias en la eficacia de reparación de los genotipos analizados (AU)


Individual response to DNA damage induced by xenobiotic agents is conditioned by the efficiency of DNA repair systems. Some of the genetic polymorphisms described in DNA repair enzymes may affect the function of these proteins, and thus determine a modified susceptibility to the exposure to environmental agents. The purpose of the present study was to investigate if the most frequent allelic variants of the DNA repair genes XRCC1 ( Arg194Trp and Arg399Gln ), XRCC3 ( Thr241Met ) or APE1 ( Asp148Glu ) might alter the DNA damage induced by styrene and its principal metabolite, styrene-7,8- oxide (SO), in human leukocytes in vitro . Peripheral leukocytes from 30 healthy volunteers were treated with styrene or SO, and induced DNA damage was evaluated by the comet assay. After styrene treatment, carriers of XRCC1 399Gln and XRCC3 241Met alleles displayed higher level of DNA breakage, suggesting lesser efficiency of the DNA repair systems. In contrast, APE1 148Glu carriers showed significantly lower styreneinduced DNA damage than the 148 Asp/Asp individuals. Nevertheless, no significant effect was obtained in cells exposed to SO, probably due to the fact that the initially induced DNA damage is greater and because small differences in the repair efficiency of the selected genotypes are not manifested (AU)


Assuntos
Análise do Polimorfismo de Comprimento de Fragmentos Amplificados/métodos , Estireno/toxicidade , Dano ao DNA , Mutação , Sistema Enzimático do Citocromo P-450/toxicidade , Ensaio Cometa/métodos , Ensaio Cometa , Técnicas de Genotipagem/instrumentação , Técnicas de Genotipagem/métodos , Análise de Variância
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