RESUMO
Currently, there is a need for fast and sensitive analytical methods for monitoring metals in water due to the progressive increase in the presence of metal ions in the environment. These metals reach the environment mainly from industrial activity and heavy metals are non-biodegradable. The present work evaluates different polymeric nanocomposites to carry out the simultaneous electrochemical determination of Cu, Cd, and Zn in water samples. Screen-printed carbon electrodes (SPCE) were modified with the nanocomposites, which were obtained by a mixture of graphene, graphite oxide, and polymers, such as polyethyleneimide, gelatin, and chitosan. These polymers have amino groups in their matrix, giving the nanocomposite the ability to retain divalent cations. However, the availability of these groups plays a fundamental role in the retention of these metals. The modified SPCEs were characterized by scanning electron microscopy, Fourier-transform infrared spectroscopy, electrochemical impedance spectroscopy, and cyclic voltammetry. The electrode that presented the best performance was selected to determine the concentration of metal ions in water samples by square-wave anodic stripping voltammetry. The obtained detection limits were 0.23 µg L-1, 0.53 µg L-1, and 1.52 µg L-1 for Zn(II), Cd(II), and Cu(II), respectively, with a lineal range of 0.1-50 µg L-1. The obtained results made it possible to conclude that the method developed using the SPCE modified with the polymeric nanocomposite presented adequate LODs, reasonable sensitivity, selectivity, and reproducibility. Besides, this platform is an excellent tool for developing devices to simultaneously determine heavy metals in environmental samples.
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Introducción: La glomerulonefritis aguda pos infecciosa (GNPI) puede cursar con complicaciones como la encefalopatía hipertensiva en 7-11% de los casos. Objetivo : determinar la frecuencia y características de la encefalopatía hipertensiva (EH) secundaria a GNPI en pacientes internados en el Departamento de Pediatría del Hospital Nacional en el periodo enero/2000-diciembre/2018. Materiales y Métodos : Estudio observacional, descriptivo, retrospectivo de pacientes con síndrome nefrítico (SN) con C3 disminuido y normalización a los tres meses, con hipertensión arterial (HTA) severa acompañada de manifestaciones neurológicas (cefalea, náuseas, vómitos, alteración de conciencia, convulsiones), que cedieron al regularizarse la HTA. Se estudiaron las características sociodemográficas (edad, sexo, procedencia, escolaridad de los padres, número de hijos) y clínicas (edema periférico, edema agudo de pulmón, hematuria, y manifestaciones neurológicas). Los datos fueron analizados utilizando estadística descriptiva mediante EPIINFO (CDC, Atlanta), expresando las variables cuantitativas como mediana y rango intercuartílico (RIC) y las cualitativas como frecuencia absoluta y porcentual. Resultados: 27 /160 (16,8%) pacientes, desarrollaron EH. La edad varió entre 3 a 16 años (mediana: 10 años; RIC: 5); el antecedente infeccioso más frecuente fue piodermitis (40,7%), seguido de faringitis aguda (37%). Todos los pacientes presentaron edema periférico y cefalea intensa. La duración de la HTA tuvo una mediana de 5 días (RIC: 4) y los días de internación una mediana de 7 (RIC: 6). Ningún paciente requirió diálisis ni quedó con secuelas, no se registraron óbitos. Conclusión: en pacientes con EH debe considerarse el diagnóstico de GNPI, investigando antecedentes infecciosos y valorando adecuadamente la volemia.
Introduction: Acute post-infectious glomerulonephritis (APGN) can present with complications such as hypertensive encephalopathy in 7-11% of cases. Objective: to determine the frequency and characteristics of hypertensive encephalopathy (HE) secondary to APGN in patients admitted to the Department of Pediatrics of the National Hospital from January/2000 to December/2018. Materials and Methods: This was an observational, descriptive and retrospective study of patients with nephritic syndrome (NS) with decreased C3 and normalization at three months, with severe arterial hypertension (AHT) accompanied by neurological manifestations (headache, nausea, vomiting, altered consciousness, seizures), which subsided when the AHT was controlled. Sociodemographic (age, sex, place of residence, parental education level, number of children in home) and clinical (peripheral edema, acute pulmonary edema, hematuria, and neurological manifestations) characteristics were studied. The data were analyzed using descriptive statistics through EPI INFO (CDC, Atlanta), expressing the quantitative variables as median and interquartile range (IQR) and the qualitative ones as absolute frequency and percentage. Results: 27/160 (16.8%) patients developed HE. Age ranged from 3 to 16 years (median: 10 years; IQR: 5); the most frequent infectious history was pyodermitis (40.7%), followed by acute pharyngitis (37%). All patients presented peripheral edema and severe headache. The duration of AHT had a median of 5 days (IQR: 4) and the days of hospitalization a median of 7 (IQR: 6). No patient required dialysis or was left with sequelae, no deaths were recorded. Conclusion: in patients with HE, the diagnosis of APGN should be considered, a history of infections obtained and adequately assessing fluid status.
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Cadmium (Cd) is one of the most dangerous heavy metals that exists. A prolonged exposure to Cd causes toxic effects in a variety of tissues, including Central Nervous System (CNS), where it can penetrate the Blood Brain Barrier (BBB). Cd exposure has been linked to neurotoxicity and neurodegenerative diseases. Soy isoflavones have a strong antioxidant capacity, and they have been shown to have positive effects on cognitive function in females. However, the mechanisms underlying Cd neurotoxicity remain completely unresolved. The purpose of this study was to characterize the potential protective effect of a soy-based diet vs. a casein-based diet against Cd toxicity in rat cerebellum. Female Wistar rats were fed with casein (Cas) or soybean (So) as protein sources for 60 days. Simultaneously, half of the animals were administered either 15 ppm of Cadmium (CasCd and SoCd groups) in water or regular tap water as control (Cas and So groups). We analyzed Cd exposure effects on trace elements, oxidative stress, cell death markers, GFAP expression and the histoarchitecture of rat cerebellum. We found that Cd tissue content only augmented in the Cas intoxicated group. Zn, Cu, Mn and Se levels showed modifications among the different diets. Expression of Nrf-2 and the activities of CAT and GPx decreased in Cas and So intoxicated groups,while 3-NT expression increased only in the CasCd group. Morphometry analyses revealed alterations in the purkinje and granular cells morphology, decreased number of granular cells and reduced thickness of the granular layer in Cd-intoxicated rats, whereas no alterations were observed in animals under a So diet. In addition, mRNA expression of apoptotic markers BAX/Bcl-2 ratio and p53 expression increased only in the CasCd group, a finding confirmed by positive TUNEL staining in the cerebellum granule cell layer in the same group. Also, Cd intoxication elicited overexpression of GFAP by astrocytes, which was prevented by soy. White matter alterations were only subtle and characterized by intramyelinic edema in the CasCd group. Overall, these results unmask an irreversible toxic effect of a subchronic Cd intoxication on the cerebellum, and identify a protective role by a soy-based diet with potential as a therapeutic strategy for those individuals exposed to this dangerous environmental contaminant.
Assuntos
Cádmio , Oligoelementos , Ratos , Feminino , Animais , Cádmio/farmacologia , Glycine max , Oligoelementos/farmacologia , Ratos Wistar , Caseínas/metabolismo , Caseínas/farmacologia , Antioxidantes/farmacologia , Dieta , Estresse Oxidativo , HomeostaseRESUMO
Cadmium (Cd) is a toxic metal and an important environmental contaminant. We analyzed its effects on oligoelements, oxidative stress, cell death, Hsp expression and the histoarchitecture of rat lung under different diets, using animal models of subchronic cadmium intoxication. We found that Cd lung content augmented in intoxicated groups: Zn, Mn and Se levels showed modifications among the different diets, while Cu showed no differences. Lipoperoxidation was higher in both intoxicated groups. Expression of Nrf-2 and SOD-2 increased only in SoCd. GPx levels showed a trend to increase in Cd groups. CAT activity was higher in intoxicated groups, and it was higher in Soy groups vs. Casein. LDH activity in BAL increased in CasCd and decreased in both soy-fed groups. BAX/Bcl-2 semiquantitative ratio showed similar results than LDH activity, confirmed by Caspase 3 immunofluorescence. The histological analysis revealed an infiltration process in CasCd lungs, with increased connective tissue, fused alveoli and capillary fragility. Histoarchitectural changes were less severe in soy groups. Hsp27 expression increased in both intoxicated groups, while Hsp70 only augmented in SoCd. This show that a soy-diet has a positive impact upon oxidative unbalance, cell death and morphological changes induced by Cd and it could be a good alternative strategy against Cd exposure.
Assuntos
Antioxidantes , Cádmio , Animais , Antioxidantes/farmacologia , Cádmio/metabolismo , Morte Celular , Dieta , Pulmão , Estresse Oxidativo , Ratos , Glycine maxRESUMO
Thousands of deaths associated with air pollution each year could be prevented by forecasting the behavior of factors that pose risks to people's health and their geographical distribution. Proximity to pollution sources, degree of urbanization, and population density are some of the factors whose spatial distribution enables the identification of possible influence on the presence of respiratory diseases (RD). Currently, Bogotá is among the cities with the poorest air quality in Latin America. Specifically, the locality of Kennedy is one of the zones in the city with the highest recorded concentration levels of local pollutants over the last 10 years. From 2009 to 2016, there were 8619 deaths associated with respiratory and cardiovascular diseases in the locality. Given these characteristics, this study set out to identify and analyze the areas in which the primary socioeconomic and environmental conditions contribute to the presence of symptoms associated with RD. To this end, information collected in field by performing georeferenced surveys was analyzed through geostatistical and machine learning tools which carried out cluster and pattern analyses. Random forests and AdaBoost were applied to establish hot spots where RD could occur, given the conjugation of predictor variables in the micro-territory. It was found that random forests outperformed AdaBoost with 0.63 AUC. In particular, this study's approach applies to densely populated municipalities with high levels of air pollution. In using these tools, municipalities can anticipate environmental health situations and reduce the cost of respiratory disease treatments.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Ambientais , Doenças Respiratórias , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Cidades/epidemiologia , Colômbia/epidemiologia , Monitoramento Ambiental , Humanos , Incidência , Material Particulado/análise , Doenças Respiratórias/epidemiologiaRESUMO
Resumen Introducción. El Zinc (Zn) es un oligoelemento esencial con gran importancia nutricional e indispensable para el crecimiento normal y la reproducción. Su deficiencia produce anormalidades fisiológicas y estructurales. Así mismo, ingerido en altas concentraciones produce efectos tóxicos, de allí la importancia de su determinación. El agua puede contribuir significativamente a la ingesta diaria de elementos trazas, entre ellos Zn. En el presente estudio se analizó el aporte de Zn en muestras de aguas de ríos y de red (de suministro público) de la provincia de San Luis y en agua mineral natural envasada, por medio de fluorescencia en fase sólida (FFS). Materiales y método.La determinación cuantitativa de Zn en muestras de agua y estándares se basó en la complejación del Zn utilizando una mezcla de o-fenantrolina y eosina a pH 7,5. Luego, una microzona de papel de filtro Blue Ribbon se impregna con la mezcla durante 1 minuto (n=6). Posteriormente, los papeles de filtro se secaron a temperatura ambiente y se colocan en una celda de cuarzo convencional adaptada para FFS. Los resultados obtenidos fueron comparados con la técnica de espectrometría de masas con plasma acoplado inductivamente. Resultados. Las muestras de agua de río analizadas presentaron valores por debajo del límite máximo de Zn recomendado por la Ley Nacional 24051, para la protección de la vida acuática. Las concentraciones de Zn en las muestras de agua de consumo analizadas (de red y envasadas) también estuvieron por debajo de los límites máximos permitidos por el Código Alimentario Argentino y la OMS. Por otro lado, se obtuvo buena concordancia entre las metodologías utilizadas. Conclusiones. El contenido de Zn de las muestras analizadas se encuentra por debajo de los valores máximos permitidos por los distintos organismos de regulación. Las muestras de agua analizadas no contribuyen a satisfacer la ingesta diaria recomendada y presentan valores considerablemente menores a los encontrados en otras regiones. Finalmente, el método aplicado mostró ser una alternativa rápida y sensible para la determinación de Zn en muestras de agua.
Abstract Introduction. Zinc (Zn) is an essential trace element with great nutritional importance and indispensable for normal growth and reproduction. Its deficiency produces physiological and structural abnormalities. Also, if ingested in high concentrations, it produces toxic effects; this is why its determination is very important. Water can contribute significantly to the daily intake of trace elements, including Zn. In this work, Zn concentration was analyzed in river and tap water samples of the province of San Luis and in bottled natural mineral water, by means of solid phase fluorescence (SPF). Materials and method. The quantitative determination of Zn in water samples and standards was based on the complexation of Zn using a mixture of o-phenanthroline and eosin at pH 7.5. Then, a microzone of Blue Ribbon filter paper was impregnated with the mixture for 1 minute (n=6). After this, the filter papers were dried at room temperature and placed in a conventional quartz cell adapted for SPF. The results obtained were compared with the Inductively Coupled Plasma - Mass Spectrometry (ICP-MS) technique. Results. The river water samples analyzed were found below the maximum limit of Zn recommended by National Law 24051 for the protection of aquatic life. The Zn concentrations in the analyzed drinking water samples (tap and bottled water) were also below the maximum limits allowed by the CAA and WHO. Furthermore, a good agreement was obtained between the methodologies used. Conclusions. The Zn content in analyzed samples was below the maximum values allowed by different regulatory organizations. The water samples analyzed do not contribute to satisfying the recommended daily intake and have considerably lower values than those found in other regions. Finally, the method applied proved to be a fast and sensitive alternative for the determination of Zn in water samples.
Assuntos
Zinco , Água Potável , Elementos Químicos , ToxicidadeRESUMO
The chloride channels, sodium and bicarbonate channels, and aquaporin water channels are coordinated to maintain the airway surface liquid that is necessary for mucociliary clearance. The general mechanism for the transport of electrolytes and fluids depends mainly on the differential expression and distribution of ion transporters and pumps. Ions and water move through the paracellular or transcellular pathways. The transcellular route of electrolyte transport requires an active transport (dependent on ATP) or passive (following electrochemical gradients) of ions. The paracellular pathway is a passive process that is ultimately controlled by the predominant transepithelial electrochemical gradients. Cystic fibrosis is a hereditary disease that is produced by mutations in the gene that encode cystic fibrosis transmembrane conductance regulatory protein (CFTR) that acts as a chloride channel and performs functions of hydration of periciliary fluid and maintenance of luminal pH. The dysfunction of the chlorine channel in the respiratory epithelium determines an alteration in the bronchial secretions, with an increase in its viscosity and alteration of the mucociliary clearance and that associated with infectious processes can lead to irreversible lung damage. CFTR dysfunction has also been implicated in the pathogenesis of acute pancreatitis, chronic obstructive pulmonary disease, and bronchial hyperreactivity in asthma. There are drugs that exploit physiological mechanisms in the transport of ions with a therapeutic objective.
Los canales de cloruros, de sodio, de bicarbonato y los de agua (aquaporinas) se coordinan para mantener la cubierta líquido superficial de las vías respiratorias, que es necesaria para el aclaramiento mucociliar. El mecanismo general para el transporte de electrolitos y agua depende principalmente de la expresión diferencial y distribución de los transportadores y bombas de iones. Los iones y el agua se mueven a través de las vía paracelular o transcelular. La ruta transcelular del transporte de electrolitos requiere un transporte activo (dependiente de ATP) o pasivo (siguiendo gradientes electroquímicos) de iones. La ruta paracelular es un proceso pasivo que está controlado, en última instancia, por los gradientes electroquímicos transepiteliales predominantes. La fibrosis quística es una enfermedad hereditaria que se produce por mutaciones en el gen que codifica la proteína reguladora de la conductibilidad transmembrana de la fibrosis quística (CFTR) que actúa como un canal de cloro y cumple funciones de hidratación del líquido periciliar y mantenimiento del pH luminal. La disfunción del canal de cloro en el epitelio respiratorio determina una alteración en las secreciones bronquiales, con aumento de su viscosidad y alteración de la depuración mucociliar y que asociado a procesos infecciosos puede conducir a daño pulmonar irreversible. La disfunción del CFTR, también se ha visto implicado en la patogénesis de la pancreatitis aguda, en la enfermedad pulmonar obstructiva crónica y la hiperreactividad en el asma. Existen fármacos que aprovechan los mecanismos fisiológicos en el transporte de iones, con un objetivo terapéutico.
Assuntos
Transporte Biológico Ativo/fisiologia , Canais de Cloreto/metabolismo , Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo , Fibrose Cística/metabolismo , Transporte de Íons/fisiologia , Depuração Mucociliar/fisiologia , Canais de Cloreto/fisiologia , Fibrose Cística/fisiopatologia , Regulador de Condutância Transmembrana em Fibrose Cística/fisiologia , HumanosRESUMO
Los canales de cloruros, de sodio, de bicarbonato y los de agua (aquaporinas) se coordinan para mantener la cubierta líquido superficial de las vías respiratorias, que es necesaria para el aclaramiento mucociliar. El mecanismo general para el transporte de electrolitos y agua depende principalmente de la expresión diferencial y distribución de los transportadores y bombas de iones. Los iones y el agua se mueven a través de las vía paracelular o transcelular. La ruta transcelular del transporte de electrolitos requiere un transporte activo (dependiente de ATP) o pasivo (siguiendo gradientes electroquímicos) de iones. La ruta paracelular es un proceso pasivo que está controlado, en última instancia, por los gradientes electroquímicos transepiteliales predominantes. La fibrosis quística es una enfermedad hereditaria que se produce por mutaciones en el gen que codifica la proteína reguladora de la conductibilidad transmembrana de la fibrosis quística (CFTR) que actúa como un canal de cloro y cumple funciones de hidratación del líquido periciliar y mantenimiento del pH luminal. La disfunción del canal de cloro en el epitelio respiratorio determina una alteración en las secreciones bronquiales, con aumento de su viscosidad y alteración de la depuración mucociliar y que asociado a procesos infecciosos puede conducir a daño pulmonar irreversible. La disfunción del CFTR, también se ha visto implicado en la patogénesis de la pancreatitis aguda, en la enfermedad pulmonar obstructiva crónica y la hiperreactividad en el asma. Existen fármacos que aprovechan los mecanismos fisiológicos en el transporte de iones, con un objetivo terapéutico.
The chloride channels, sodium and bicarbonate channels, and aquaporin water channels are coordinated to maintain the airway surface liquid that is necessary for mucociliary clearance. The general mechanism for the transport of electrolytes and fluids depends mainly on the differential expression and distribution of ion transporters and pumps. Ions and water move through the paracellular or transcellular pathways. The transcellular route of electrolyte transport requires an active transport (dependent on ATP) or passive (following electrochemical gradients) of ions. The paracellular pathway is a passive process that is ultimately controlled by the predominant transepithelial electrochemical gradients. Cystic fibrosis is a hereditary disease that is produced by mutations in the gene that encode cystic fibrosis transmembrane conductance regulatory protein (CFTR) that acts as a chloride channel and performs functions of hydration of periciliary fluid and maintenance of luminal pH. The dysfunction of the chlorine channel in the respiratory epithelium determines an alteration in the bronchial secretions, with an increase in its viscosity and alteration of the mucociliary clearance and that associated with infectious processes can lead to irreversible lung damage. CFTR dysfunction has also been implicated in the pathogenesis of acute pancreatitis, chronic obstructive pulmonary disease, and bronchial hyperreactivity in asthma. There are drugs that exploit physiological mechanisms in the transport of ions with a therapeutic objective.
Assuntos
Humanos , Transporte Biológico Ativo/fisiologia , Depuração Mucociliar/fisiologia , Transporte de Íons/fisiologia , Canais de Cloreto/metabolismo , Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo , Fibrose Cística/metabolismo , Canais de Cloreto/fisiologia , Regulador de Condutância Transmembrana em Fibrose Cística/fisiologia , Fibrose Cística/fisiopatologiaRESUMO
Cadmium (Cd) is a carcinogen with several well-described toxicological effects in humans, but its molecular mechanisms are still not fully understood. Overexpression of heat shock protein 27 (HSP27/HSPB1)-a multifunctional protein chaperone-has been shown to protect cells from oxidative damage and apoptosis triggered by Cd exposure. The aims of this work were to investigate the potential use of extracellular recombinant HSP27 to prevent/counteract Cd-induced cellular toxicity and to evaluate if peroxynitrite was involved in the development of Cd-induced toxicity. Here, we report that the harmful effects of Cd correlated with changes in oxidative stress markers: upregulation of reactive oxygen species, reduction in nitric oxide (NO) bioavailability, increment in lipid peroxidation, peroxynitrite (PN), and protein nitration; intracellular HSP27 was reduced. Treatments with Cd (100 µM) for 24 h or with the peroxynitrite donor, SIN-1, decreased HSP27 levels (~50%), suggesting that PN formation is responsible for the reduction of HSP27. Pre-treatments of the cells either with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) (a pharmacological inhibitor of NO synthase) or with recombinant HSP27 (rHSP27) attenuated the disruption of the cellular metabolism induced by Cd, increasing in a 55 and 52%, respectively, the cell viability measured by CCK-8. Cd induced necrotic cell death pathways, although apoptosis was also activated; pre-treatment with L-NAME or rHSP27 mitigated cell death. Our findings show for the first time a direct relationship between Cd-induced toxicity and PN production and a role for rHSP27 as a potential therapeutic agent that may counteract Cd toxicity.
Assuntos
Cádmio/toxicidade , Proteínas de Choque Térmico HSP27/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Movimento Celular/efeitos dos fármacos , Feminino , Corantes Fluorescentes/química , Proteínas de Choque Térmico HSP27/genética , Proteínas de Choque Térmico HSP27/farmacologia , Células HeLa , Humanos , Microscopia de Fluorescência , NG-Nitroarginina Metil Éster/farmacologia , Óxido Nítrico/metabolismo , Ácido Peroxinitroso/análise , Ácido Peroxinitroso/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Proteínas Recombinantes/biossíntese , Proteínas Recombinantes/isolamento & purificação , Proteínas Recombinantes/farmacologia , Regulação para Cima/efeitos dos fármacos , Neoplasias do Colo do Útero/metabolismo , Neoplasias do Colo do Útero/patologiaRESUMO
[{"text": "Objetivo: determinar la relación entre hábitos alimentarios y la presencia de síntomas digestivos altos en estudiantes de la Universidad Nacional de San Luis. Metodología: estudio transversal descriptivo, en el cual participaron 150 sujetos (mujeres = 86, hombres = 64), estudiantes de 20 a 30 años de edad, de la Universidad Nacional de San Luis, sede San Luis; se utilizó una encuesta validada del Ministerio de Desarrollo Social de Argentina, adaptada a los fines de la presente investigación. Resultados: la mayoría de los estudiantes consume casi siempre las cuatro comidas principales; las formas de cocción predominantes fueron: horno, plancha y hervido. Se observó escasa y poco variada selección de frutas y verduras, un consumo ocasional de bebidas alcohólicas y de productos ricos en grasas, sal y azúcares. La elección de dulces y azúcares, mate cebado, té y café fue elevada. Los síntomas más recurrentes fueron: distensión abdominal, hambre dolorosa, regurgitación, náuseas y pirosis; los que menos aparecieron fueron vómito y anorexia. Los estudiantes asociaron la recurrencia de los síntomas al consumo de comidas con salsa, comidas picantes, mate cebado, té y café. En el sexo masculino, las bebidas alcohólicas también se asociaron a la sintomatología digestiva. Conclusiones: se pudo observar la presencia de más de un síntoma digestivo alto simultáneo en cada estudiante, unido a la presencia de hábitos alimentarios perjudiciales. Por ello, es indispensable impartir educación alimentaria nutricional.", "_i": "es"}, {"text": "Objective: To determine the relationship between the eating habits and the presence of upper digestive problems of 150 university students. Methodology: This is a descriptive cross-sectional study in which 150 individuals participated (86 females, 64 males). The students ranged from 20 to 30 years of age and were from the Universidad Nacional de San Luis. The study used a survey validated by the Ministry of Social Development of Argentina, which was adapted to the purposes of the present investigation. Results: The majority of the students almost always consumed four main meals, the main methods of cooking were: to bake, to grill and to boil. It was observed that there was hardly any variety in the selection of fruits and vegetables, in the occasional consumption of alcoholic drinks or in food products rich in fat, salt and sugar. The choice of sweets and sugars, mate "cebado" tea and coffee was high. The most recurring symptoms were: stomach distension, painful hunger, regurgitation, nausea, and heartburn. Those symptoms that occurred less were vomiting and anorexia. The students associated the recurrences of symptoms with the consumption of these fares: foods with sauce, spicy meals, mate "cebado", tea and coffee. In males, alcoholic beverages were also associated with digestive problems. Conclusions: It was possible simultaneously to observe the presence of more than one upper digestive problem in each of the students in correlation to harmful eating habits. For this reason, it is essential to provide education in nutritional eating.", "_i": "en"}, {"text": "Objetivo: determinar a relação entre hábitos alimentares dos alunos da Universidade Nacional de San Luis e a presença de sintomas digestivos superiores. Metodologia: estudo descritivo, transversal, em que participaram 150 estudantes (femininos = 86, masculinos = 64) de 20 a 30 anos de idade, da Universidade Nacional de San Luis, sede San Luis, usando um inquérito validado pelo Ministério do Desenvolvimento Social da Argentina, adaptado aos fins da presente investigação. Resultados: a maioria dos estudantes realiza quase sempre as quatro principais refeições, as formas de cocção predominantes foram: forno, na chapa e fervido. Observou-se escasso e pouco variado consumo de frutas e vegetais, um consumo ocasional de bebidas alcoólicas e produtos ricos em gorduras, sal e açúcares. O consumo de doces e açúcares, chimarrão, chá e café foram elevados. Os sintomas mais frequentes foram: distensão abdominal, fome dolorosa, regurgitação, náuseas e pirose, e os que menos apareceram foram: vômito e anorexia. Os estudantes associaram a recorrência dos sintomas ao consumo de: comidas com molho, comidas picantes, chimarrão, chá e café. No sexo masculino, as bebidas alcoólicas foram também associadas à sintomatologia digestiva. Conclusões: observou-se a presença de mais de um sintoma simultaneamente em cada estudante e, por sua vez, a prática de comportamentos alimentares prejudiciais para eles mesmos. Portanto, é essencial a realização de educação alimentar nutricional.", "_i": "pt"}]
Assuntos
Humanos , Masculino , Feminino , Trato Gastrointestinal , Comportamento Alimentar , Estudantes , Dieta SaudávelRESUMO
Increased chicken-derived fat and fructose consumption in the human diet is paralleled by an increasing prevalence of obesity and metabolic syndrome (MS). Herein, we aimed at developing and characterizing a mouse model of diet-induced obesity (DIO) resembling most of the key features of the human MS. To accomplish this, we fed male C57BL/6J mice for 4, 8, 12, and 16 weeks with either a low-fat diet (LFD) or a high-chicken-fat diet (HFD) and tap water with or without 10% fructose (F). This experimental design resulted in the following four experimental groups: LFD, LFD + F, HFD, and HFD + F. Over the feeding period, and on a weekly basis, the HFD + F group had more caloric intake and gained more weight than the other experimental groups. Compared to the other groups, and at the end of the feeding period, the HFD + F group had a higher adipogenic index, total cholesterol, low-density lipoprotein cholesterol, fasting basal glycemia, insulin resistance, hypertension, and atherogenic index and showed steatohepatitis and systemic oxidative stress/inflammation. A mouse model of DIO that will allow us to study the effect of MS in different organs and systems has been developed and characterized.
RESUMO
Suboptimal intake of Zinc (Zn) is one of the most common worldwide nutritional problems. The aim of this study is to provide new evidence on the relation between moderate Zn restriction, and cytoprotective functions in airway epithelium. We analyzed the effect of moderate Zn deficiency (ZD) on the expression of several pro and anti-apoptotic proteins and cytoprotective factors (Hsp27 and Hsp 70i), as well as the effect of restoring Zn during the refeeding period. Adult male rats were divided into three groups: Zn-adequate control group, Zn-deficient group and Zn-refed group. Our previous findings showed an important oxidative and nitrosative stress during ZD, this situation is accompanied by inflammation and alterations in the expression of matrix extracellular proteins. We observed a strong immunopositive area of anti and pro-apoptotics proteins in ZD groups. The mRNA levels of Nrf-2, Bax and Bad were increased in ZD, while in ZD refed group its levels were similar to the control values. The increased expression of Nrf-2 is likely to be critical for protection of lung under inflammatory process triggered during ZD. Hsp27 and Hsp 70i showed an increase of immunostaining area but they were not significant. During the supplementation period, heat-shock proteins increased significantly. In conclusion, our results provide further evidence of the pathways involved in cytoprotection and apoptosis caused by ZD. Additional studies are required in order to investigate whether Hsp27 and Hsp70 are consistently associated with cellular stress and inflammation in lung. There may be a beneficial role for improved Zn nutrition or Zn supplements early in lung pathology.
Assuntos
Citoproteção , Células Epiteliais/citologia , Pulmão/citologia , Zinco/deficiência , Animais , Apoptose/efeitos dos fármacos , Citoproteção/genética , Dieta , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Proteínas de Choque Térmico HSP27/análise , Proteínas de Choque Térmico HSP27/biossíntese , Proteínas de Choque Térmico HSP70/análise , Proteínas de Choque Térmico HSP70/biossíntese , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Masculino , Ratos , Ratos Wistar , Zinco/administração & dosagem , Zinco/farmacologiaRESUMO
Suboptimal intake of Zn is one of the most common nutritional problems worldwide. Previously, we have shown that Zn deficiency (ZD) produces oxidative and nitrosative stress in the lung of rats. We analyse the effect of moderate ZD on the expression of several intermediate filaments of the cytoskeleton, as well as the effect of restoring Zn during the refeeding period. Adult male rats were divided into three groups: Zn-adequate control (CO) group; ZD group; Zn-refeeding group. CerbB-2 and proliferating cell nuclear antigen (PCNA) expression was increased in the ZD group while the other parameters did not change. During the refeeding time, CerbB-2, cytokeratins, vimentin and PCNA immunostaining was higher than that in the CO group. The present findings indicate that the overexpression of some markers could lead to the fibrotic process in the lung. Perhaps ZD implications must be taken into account in health interventions because an inflammation environment is associated with ZD in the lung.
Assuntos
Matriz Extracelular/química , Matriz Extracelular/metabolismo , Pulmão/metabolismo , Zinco/deficiência , Animais , Biomarcadores/análise , Peso Corporal , Caderinas/química , Caderinas/metabolismo , Regulação da Expressão Gênica , Imuno-Histoquímica , Queratinas/química , Queratinas/metabolismo , Masculino , Ratos , Receptor ErbB-2/química , Receptor ErbB-2/metabolismo , Fator de Crescimento Transformador beta1/genética , Fator de Crescimento Transformador beta1/metabolismoRESUMO
Suboptimal intake of dietary zinc (Zn) is one of the most common nutritional problems worldwide. Previously, the authors have shown that zinc deficiency (ZD) produces oxidative and nitrosative stress in lung of male rats. The goal of this study is to test the effect of moderate ZD on insulin-like growth factor (IGF)-1, IGF-binding protein (IGFBP)-5, NADH oxidase (NOX)-2, tumor necrosis factor alpha (TNFalpha), as well as the effect of restoring zinc during the refeeding period. Adult male rats were divided into 3 groups: Zn-adequate control group, Zn-deficient group, and Zn-refeeding group. eNOS, metallothionein (MT) II, and NOX-2 was increased in ZD group. The authors observed an increased gene transcription of superoxide dismutase (SOD)-2 and gluthathione peroxidase (GPx)-1 in ZD group, as well as in ZD-refeeding group, but catalase (CAT) transcription did not change in the treated groups. Proinflammatory factors, such as TNFalpha and vascular cell adhesion molecular (VCAM)-1 increased in ZD, whereas it decreased in ZD refeeding. However, peroxisome proliferator-activated receptor gamma (PPARgamma) and IGF-1 gene transcription decreased in ZD, whereas IGFBP-5 decreased in the ZD group. These parameters are associated to alterations in the lung histoarchitecture. The zinc supplementation period is brief (only 10 days), but it is enough to inhibit some proinflammatory factors. Perhaps, zinc deficiency implications must be taken into account in health interventions because inflammation and prooxidant environment are associated with ZD in lung.
Assuntos
Regulação da Expressão Gênica , Inflamação/etiologia , Pulmão/patologia , Desnutrição/patologia , Estresse Oxidativo , Zinco/deficiência , Animais , Biomarcadores/análise , Perfilação da Expressão Gênica , Inflamação/diagnóstico , Inflamação/tratamento farmacológico , Pulmão/metabolismo , Masculino , Desnutrição/metabolismo , Ratos , Zinco/uso terapêuticoRESUMO
Cadmium is an environmental toxic metal implicated in human prostate carcinogenesis. The mechanism of its toxicity is not fully understood. Previously, we showed that cadmium exposure induces oxidative stress, especially lipid peroxidation. This study evaluates the effect of chronic exposure to 0.886 mM of cadmium (Cd) per liter in the drinking water on prostate lipid content and metabolism in Wistar rats. We determined the lipid profile and measured the expression of lipogenic enzymes: FAS, GPAT, LPL, DGAT-1, DGAT-2, ACO, CPT-1 and CT, and of certain factors involved in lipid regulation and fatty acid transporters: FAT/CD36, E-FABP, SREBP-2, PPAR-gamma and PPAR-alpha by RT-PCR. Ultrastructure was analyzed by electron microscopy and, as prostate is an androgen controlled gland, AR expression was measured by RT-PCR and Western blot. Cd altered the prostatic lipid profile. Triglycerides (TG) and esterified cholesterol (EC) decreased, free cholesterol (FC) and phospholipids (PL) increased and total cholesterol (TC) did not change. FAS, MDH and IDH activities did not vary but G6PDH decreased significantly in Cd group. Regarding TG synthesis, DGAT-1 decreased while GPAT increased and FAS, LPL and DGAT-2 remained unchanged. Regarding beta oxidation, CPT-1 increased while ACO expression decreased in Cd group. In the PL pathway, CT expression was increased. All these results would justify the decrease of TG in Cd group when compared to control. In the cholesterol metabolic pathway, HMGCoAR and SREBP-2 increased. PPAR-alpha increased but PPAR-gamma did not change. Regarding fatty acid transporters, FAT/CD36 decreased, while E-FABP increased. AR mRNA and protein expression decreased. Ultrastructural analysis showed a decrease in lipid droplets and signs of cellular damage in the Cd group. Cadmium exposure induces important changes in prostatic lipid profile and metabolism, confirmed by the morphology analyses, which also showed signs of cellular damage. These results could be important to further understanding the complex mechanism of cadmium toxicity in prostate and in the development of better treatments for people and animals exposed to the heavy metal.
Assuntos
Cádmio/toxicidade , Colesterol/metabolismo , Exposição Ambiental , Próstata/efeitos dos fármacos , Próstata/ultraestrutura , Triglicerídeos/metabolismo , Animais , Colesterol/biossíntese , Humanos , Masculino , Próstata/metabolismo , Próstata/patologia , Ratos , Ratos Wistar , Triglicerídeos/antagonistas & inibidores , Triglicerídeos/biossínteseRESUMO
Suboptimal intake of Zn is one of the most common nutritional worldwide problems. Previously, we showed that Zn deficiency produces alterations in lung lipid metabolism in rats. We studied the effect of a Zn-limited (ZL) diet on the expression of the enzymes involved in phosphatidylcholine and cholesterol synthesis. After 2 months of treatment with a ZL diet we found important variations in the lipid content of Wistar male rats: triacylglycerol (TG) decreased 60% (P<0.001) while esterified cholesterol (EC), free cholesterol and phospholipids (PL) increased 66%, 24 % and 25% respectively. We also observed a decrease of 40 % in the amount of (3)H incorporated into TG and an increase of 47% and 28% in the (3)H incorporated to PL and EC respectively. Fatty acid synthase and glucose-6-phosphate dehydrogenase activity was increased (P<0.01 and P<0.05 respectively). Glycerol-3-phosphate acyltransferase, lipoprotein lipase, diacyl glycerol acyl transferase and 3-hydroxy-3-methylglutaryl CoA reductase expression decreased (P<0.01 in all cases), while acetyl CoA carboxylase and cholinephosphate cytidylyltransferase increased (P<0.01 and P<0.005 respectively). These results suggest that ZL alters the expression of enzymes involved in phosphatidylcholine and cholesterol synthesis, which could lead to increased PL and cholesterol and decreased TG. This study suggests that major changes in the lipid composition of lung are induced by a ZL condition. Therefore, Zn deficiency must be taken into account in order to design therapies and public health interventions, such as Zn supplementation for high-risk subjects or certain diseases, such as asthma.
Assuntos
Colina-Fosfato Citidililtransferase/metabolismo , Dieta , Hidroximetilglutaril-CoA Redutases/metabolismo , Pulmão/metabolismo , Triglicerídeos/metabolismo , Zinco/deficiência , Animais , Peso Corporal , Colesterol/análise , Colesterol/biossíntese , Colesterol/sangue , HDL-Colesterol/sangue , Ácido Graxo Sintases/metabolismo , Marcação por Isótopo , Lipogênese , Lipase Lipoproteica/metabolismo , Pulmão/química , Pulmão/enzimologia , Masculino , Estado Nutricional , Fosfatidilcolinas/biossíntese , Fosfolipídeos/análise , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Triglicerídeos/análise , Triglicerídeos/sangue , Zinco/administração & dosagemRESUMO
Reactive oxygen and nitrogen species have been implicated in the pathogenesis of pulmonary diseases. The goal of this study was to measure the response of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 enzymes (COX-2) in lung with moderate zinc deficiency. Adult male Wistar rats were divided into two groups receiving (1) a zinc-deficient diet (ZD) or (2) a zinc-adequate control diet. After 2 months of treatment, the zinc-deficient group showed a significant pulmonary edema. This was associated to a reduction of protein thiols and to a significant increase of metallothionein and glutathione disulfide levels. In addition, a higher serum and lung NO production in ZD group was positively related to the higher activity and expression of iNOS and COX-2 found in lungs. Western blot analysis revealed increased IkappaBalpha degradation, an indicator of NF-kappaB activation in ZD lungs. Anatomopathologic analysis of ZD lungs showed an increase of connective tissue fibers with an influx of polymorphonuclear cells. These cells and type II cells from the alveoli showed specific immunohistochemical signals for iNOS. The conclusion is that, during the development of zinc-deficiency, iNOS activity increases in lung and contributes to lung injury. Zinc deficiency implications must be taken into account to design therapies and public health interventions involving targeted zinc supplementation for high-risk subjects or certain diseases, such as asthma.
Assuntos
Ciclo-Oxigenase 2/metabolismo , Pulmão/enzimologia , NF-kappa B/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Zinco/deficiência , Animais , Peso Corporal , Imuno-Histoquímica , Pulmão/metabolismo , Masculino , Tamanho do Órgão , Estresse Oxidativo , Edema Pulmonar/metabolismo , Ratos , Ratos WistarRESUMO
We evaluated whether nutritional vitamin A deficiency generates oxidative stress and inflammation in aorta. Wistar male rats (21 days old) were given free access to a control (8 mg retinol as retinyl palmitate/kg) or a vitamin A- deficient diet for three months. One group of deficient animals was fed with the control diet fifteen days before sacrifice. Thiobarbituric acid-reactive substances (TBARS) and nitrite concentration where both analyzed in serum and aorta. Aorta Copper-Zinc Superoxide dismutase (CuZnSOD), Glutathion peroxidase (GPx) and Catalase (CAT) activities were measured. In addition, binding activity of the nuclear factor- kB (NF-kB), inducible and endothelial Nitric Oxide synthase (iNOS and eNOS, respectively) and Ciclooxygenase-2 (COX-2) expressions were determinated in aorta. Rats fed the vitamin A- deficient diet were characterized by sub-clinical plasma retinol concentration and showed increased serum and aorta concentrations of TBARS compared to controls. Lower than control activities of CuZnSOD, GPx, and CAT were observed in aorta of the vitamin A- deficient group. The binding activity of NF- kB was higher in vitamin A- deficient animals than controls. In addition, NO production evaluated as nitrite concentration increased in aorta and serum, associated with a higher expression of iNOS, eNOS and COX-2 in aorta of vitamin A-deficient rats. The incorporation of vitamin A into the diet of vitamin A-deficient rats reverted the changes observed in TBARS level, CuZnSOD and GPx activities, nitrite concentration and also, iNOS, eNOS and COX-2 expression. Prooxidant environment and inflammation are induced by vitamin A deficiency in rat aorta.
Assuntos
Antioxidantes/metabolismo , Aorta/metabolismo , Aorta/patologia , Deficiência de Vitamina A/metabolismo , Deficiência de Vitamina A/patologia , Animais , Aorta/efeitos dos fármacos , Peso Corporal/efeitos dos fármacos , Inflamação/metabolismo , Inflamação/patologia , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , NF-kappa B/metabolismo , Nitratos/metabolismo , Oxirredução/efeitos dos fármacos , Ratos , Ratos Wistar , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Vitamina A/sangueRESUMO
Cadmium chloride is an environmental toxicant implicated in human prostate carcinogenesis. The mechanism of its toxicity is far from fully understood. This study evaluates the effect of exposure to an oral non-carcinogenic dose of cadmium (15 ppm in drinking water for three months) on different parameters of the ventral prostatic lobe of normal and exposed rats. We analyzed the histology by optic light microscopy, activities of antioxidant enzymes (CAT, SOD, GPx and G-6-PDH), expression of iNOS and COX-2 by Western blot, expression of MT-I, MT-II, IGF-I, IGF-BP5 and rtert by RT-PCR. Histological changes were found: the height of the cells decreased, acinar lumen were enlarged and they lost the typical invaginations. Lipoperoxidation was increased in the Cd group and the antioxidant enzymes changed their activities: SOD increased, CAT and G-6-PDH decreased and GPx did not show variations. iNOS and COX-2 did not change their expressions. MT-I and IGF-BP5 mRNA increased while MT-II, IGF-I and rtert did not show variations. Cd exposure induces important morphological changes in the prostate, which could be a consequence of lipoperoxidation and oxidative stress, which are not related to iNOS and COX-2. The histology suggests an involution state of the gland, confirmed by the expression of IGF-I, IGF-BP5 and rtert.
Assuntos
Cádmio/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Próstata/metabolismo , Próstata/patologia , Animais , Antioxidantes/metabolismo , Western Blotting , Catalase/biossíntese , Catalase/genética , Ciclo-Oxigenase 2 , Glucosefosfato Desidrogenase/biossíntese , Glucosefosfato Desidrogenase/genética , Glutationa Peroxidase/biossíntese , Glutationa Peroxidase/genética , Isoenzimas/biossíntese , Masculino , Metalotioneína/biossíntese , Metalotioneína/genética , Óxido Nítrico Sintase/biossíntese , Óxido Nítrico Sintase Tipo II , Prostaglandina-Endoperóxido Sintases/biossíntese , Próstata/efeitos dos fármacos , RNA/biossíntese , RNA/genética , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Superóxido Dismutase/biossíntese , Superóxido Dismutase/genética , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Aumento de Peso/efeitos dos fármacosRESUMO
Few studies are available about the role of dietary zinc (Zn) in respiratory diseases. Adult male rats were divided into 2 groups and fed respectively a moderate Zn-deficient diet and a Zn-adequate control diet. In lung tissue at 2 months, thiobarbituric acid-reactive species (TBARS), total glutathione, glutathione disulfide, protein carbonyls, metallothionein, and the activities of glutathione peroxidase (GPx), catalase, CuZn-superoxide dismutase (CuZnSOD) and glucose-6-phosphate dehydrogenase (G-6-PDH) were increased, but protein thiols decreased. In lung tissue at 4 months, TBARS, metallothionein, and the activities of CuZnSOD, Mn-superoxide dismutase (MnSOD) increased. The activities GPx, catalase, G-6-PDH were lower than control group. The changes were accompanied by histological alterations in Zn-deficient lung. The results provide evidence of the pro-oxidative effects of Zn-deficiency in lung, and suggest that the time of treatment play a key role in determining lung susceptibility to oxidative stress.