Dietary açai modulates ROS production by neutrophils and gene expression of liver antioxidant enzymes in rats

Açai (Euterpe oleracea Mart.) has recently emerged as a promising source of natural antioxidants. Because increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the development of diabetic complications and many health claims have been reported for açai, the present study was undertaken to evaluate the possible protective effects of açai on the production of reactive oxygen species by neutrophils and on the liver antioxidant defense system in control and streptozotocin-induced diabetic rats. Diet supplementation with 2% açai was found to increase mRNA levels for gamma-glutamylcysteine synthetase and glutathione peroxidase in liver tissue and to decrease reactive oxygen species production by neutrophils. Compared to control animals, diabetic rats exhibited lower levels of mRNA coding for Zn-superoxide dismutase, glutathione peroxidase and gamma-glutamylcysteine synthetase and higher levels of reactive oxygen species production by neutrophils, thiobarbituric acid-reactive substances and carbonyl proteins in hepatic tissues. Although açai supplementation was not effective in restore gene expression of antioxidant enzymes in diabetic rats, it showed a protective effect, decreasing thiobarbituric acid-reactive substances levels and increasing reduced glutathione content in the liver. These findings suggest that açai can modulate reactive oxygen species production by neutrophils and that it has a significant favorable effect on the liver antioxidant defense system under fisiological conditions of oxidative stress and partially revert deleterious effects of diabetes in the liver

Apuntes en torno al Sistema de Información de Apoyo a la Gestión de la Institución Educativa (SIAGIE) : recomendaciones y proyecciones para el mediano plazo

Establece lineamientos para la oportuna emisión de la normatividad pedagógica que deviene luego en el desarrollo de sistemas de información. Del mismo modo, formula y propone una definición institucional del concepto de administración de sistemas de información. Asimismo, fija las bases para la incorporación gradual en el sistema, de los procesos respectivos de la Educación Básica Especial (EBE) y de la Educación Básica Alternativa (EBA), similarmente a lo ya realizado con los procesos de Matrícula y Evaluación de la Educación Básica Regular (EBR)

Polpa de açaí modula a produção de espécies reativas de oxigênio por neutrófilos e a expressão gênica de enzimas antioxidantes em tecido hepático de ratos.

Açaí (Euterpe oleracea Mart.) recentemente foi identificado como uma fonte promissora de antioxidantes naturais. O estresse oxidativo e a redução dos mecanismos de defesa antioxidante são fatores importantes no desenvolvimento das complicações do diabetes. Assim, o objetivo do presente estudo foi avaliar o possível efeito protetor da polpa de açaí sobre a produção de espécies reativas de oxigênio (ERO) por neutrófilos e sobre o sistema de defesa antioxidante hepático em ratos controle e diabéticos. Ratas Fischer foram divididas em 4 grupos de 8 animais de acordo com o tratamento recebido, Controle (C), Açaí (A), diabético (D), e diabético + açaí (DA). O diabetes foi induzido por uma única injeção intraperitoneal de estreptozotocina (35mg/kg de peso corporal) no primeiro dia do experimento. Os grupos C e D receberam dieta padrão (AIN-93), os grupos A e DA receberam dieta padrão acrescida com 2% da polpa de açaí. Ao final de 4 semanas os animais foram anestesiados e eutanasiados. A suplementação da dieta com 2% da polpa de açaí por 30 dias aumentou os níveis de mRNA para γ-glutamilcisteína sintetase (γ-GCS) e glutationa peroxidase (GPx) no tecido hepático, aumentou o conteúdo de glutationa total e reduziu a produção de EROs por neutrófilos em ratos controle. Os ratos diabéticos apresentaram redução na expressão de mRNA que codificam para a Zn-superóxido dismutase (Zn-SOD), GPx and γ-GCS e aumento nos níveis de substâncias reativas ao ácido tiobarbitúrico (TBARS) e proteínas carboniladas quando comparado aos ratos controle. A suplementação com a polpa de açaí não alterou a expressão de enzimas antioxidantes em ratos diabéticos, no entanto apresentou efeito protetor, através da redução da peroxidação lipídica e aumento de glutationa total no fígado desses animais. Esses resultados sugerem que a polpa de açaí pode modular a produção de ROS por neutrófilos a apresentar efeito favorável sobre o sistema de defesa antioxidante hepático.Açai (Euterpe oleracea Mart.) has recently been identified as a promising source of natural antioxidants. Because increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the development of diabetic complications, the present study was undertaken to evaluate the possible protective effects of açai on the production of reactive oxygen species (ROS) by neutrophils and on the liver antioxidant defense system in control and streptozotocin-induced diabetic rats. Female Fischer rats were divided into four groups, control (C), açai (A), diabetic (D), diabetic + açai (DA). Diabetes was induced by a single intraperitoneal injection of streptozotocin (35 mg/kg body weight). Animals in groups C and D were fed a standard diet (AIN-93); those in groups A and DA were given the standard diet with 2% (w/w) açai pulp added for 30 days. Supplementation of the diet with 2% açai for 30 days was found to increase levels of mRNA for gamma-glutamylcysteine synthetase (γ-GCS) and glutathione peroxidase (GPx) in liver tissue, to increase the glutathione (GSH) content of the liver and to decrease ROS production by neutrophils. Compared to control animals, diabetic rats exhibited lower levels of mRNA coding for Zn-superoxide dismutase (Zn-SOD), GPx and γ-GCS and higher levels of thiobarbituric acid-reactive substances (TBARS) and carbonyl proteins in hepatic tissues. Although açai supplementation did not change the level of expression of mRNAs coding for antioxidant enzymes in diabetic rats, it showed a protective effect, decreasing lipid peroxidation and increasing GSH content in the liver. These findings suggest that açai can modulate ROS production by neutrophils and that it has a significant favorable effect on the liver antioxidant defense system

Efeito protetor do açaí (Euterpe oleracea Mart.) sobre a esteatose hepática, resistência à insulina e estresse oxidativo induzidos por dieta hiperlipídica em camundongos.

Programa de Pós-Graduação em Ciências Biológicas. Núcleo de Pesquisas em Ciências Biológicas, Pró-Reitoria de Pesquisa de Pós Graduação, Universidade Federal de Ouro Preto.A crescente incidência da obesidade e comorbidades associadas está relacionada a um aumento paralelo da Doença Hepática Gordurosa não Alcoólica (NAFLD), uma das mais frequentes causas de doença crônica do fígado da atualidade. A NAFLD representa um espectro de condições caracterizadas por acúmulo de triacilgliceróis nos hepatócitos, que incluem a esteatose, esteato-hepatite, que pode evoluir para cirrose e carcinoma hepatocelular. Embora sua patogênese exata permaneça desconhecida, a hipótese mais aceita define que alterações metabólicas desencadeadas pela resistência à insulina levam ao desenvolvimento da esteatose hepática, considerada o primeiro evento, seguido do estresse oxidativo que contribui para a evolução do quadro. Compostos bioativos presentes em alimentos, principalmente polifenóis têm sido considerados promissores na prevenção de distúrbios metabólicos. O açaí (Euterpe oleracea Mart.) ganhou reconhecimento internacional devido ao seu alto conteúdo de polifenóis e capacidade antioxidante. Assim, o objetivo do presente estudo foi avaliar os efeitos do consumo de um extrato aquoso de açai (EAA) sobre alterações metabólicas desencadeadas pelo consumo de dieta hiperlipídica em camundongos. Camundongos Swiss machos foram divididos inicialmente em 2 grupos experimentais, um grupo (C) recebeu dieta padrão AIN-93M, e o outro grupo (HF) recebeu uma dieta hiperlipídica (32% de banha suína e 1% de colesterol) por seis semanas, após este período, os grupos C e HF foram subdivididos em quatro grupos de acordo com o tratamento recebido. Os grupos C e CA receberam dieta padrão, e os grupos HF e HFA receberam dieta hiperlipídica, os grupos CA e HFA receberam tratamento com o EAA (3g/Kg de peso corporal), administrado diariamente via gavagem por mais seis semanas. Camundongos do grupo HF apresentaram maior ganho de massa corporal associado à resistência à insulina, alterações no perfil das adipocinas TNFα e adiponectina, hepatomegalia, elevação dos níveis séricos das transaminases e esteatose hepática. Além disso, apresentaram alterações nos níveis de mRNA de genes relacionados ao metabolismo de lipídios hepático e aumento no estresse oxidativo. O tratamento com o EAA apresentou efeito protetor sobre a esteatose hepática, através da melhora nos níveis de adipocinas, sensibilidade a insulina e aumento na expressão dos genes relacionados a β-oxidação de ácidos graxos mediada por PPAR-α. E ainda, promoveu uma melhora no balanço oxidante/antioxidante hepático. Estes dados indicam que o açaí pode representar uma estratégia dietética viável, associada a prevenção e/ou tratamento de distúrbios metabólicos.The worldwide rising prevalence of obesity and its comorbidities is associated with a parallel increase in nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disease. The spectrum of NAFLD ranges from simple steatosis to steatohepatitis, which can progress to end-stage liver disease. Although its exact pathogenesis is still unknown, the most widely accepted hypothesis states that metabolic alterations induced by the insulin resistance leads to the development of hepatic steatosis considered the first event, followed by oxidative stress that contributes to the progression of the disease. Phytochemicals in foods, especially polyphenols have been considered promising in preventing metabolic disorders. Açaí (Euterpe oleracea Mart.) has gained worldwide popularity and has been recognized as one of the new “super fruits” due to its high polyphenol content and antioxidant properties. This study was designed to investigate the effects of consumption of an aqueous extract of acai (EAA) on metabolic changes triggered by the consumption of high-fat diet in mice. Swiss mice were fed a control AIN-93M, or high-fat diet (HFD). After six weeks, mice were assigned to one of the two treatment conditions, water or açai at 3 g/Kg, orally administered by gavage for an additional six weeks. Mice fed with HFD showed higher body mass gain associated with insulin resistance, altered profile of adipokines TNFα and adiponectin, hepatomegaly, elevated serum transaminase levels and hepatic steatosis. Furthermore, exhibited changes in the mRNA levels of genes related to metabolism of hepatic lipids and increased oxidative stress. Treatment with AAE showed a protective effect on hepatic steatosis, through the improvement in adipokines levels, insulin sensitivity and increased expression of genes related to PPARα-mediated fatty acid oxidation. Additionally, promoted an improvement in the balance oxidant / antioxidant liver. These findings indicate that açai may represent a viable dietary strategy associated with the treatment and or prevention of metabolic disorders

Iron dextran increases hepatic oxidative stress and alters expression of genes related to lipid metabolism contributing to hyperlipidaemia in murine model.

The objective of this study was to investigate the effects of iron dextran on lipid metabolism and to determine the involvement of oxidative stress. Fischer ratswere divided into two groups: the standard group (S),whichwas fed the AIN-93Mdiet, and the standard plus iron group (SI), which was fed the same diet but also received iron dextran injections. Serum cholesterol and triacylglycerol levels were higher in the SI group than in the S group. Iron dextran was associated with decreased mRNA levels of ppar, and its downstream gene cpt1a, which is involved in lipid oxidation. Iron dextran also increased mRNA levels of apoB-100, MTP, and LFABP indicating alterations in lipid secretion. Carbonyl protein and TBARS were consistently higher in the liver of the iron-treated rats. Moreover, a significant positive correlation was found between oxidative stress products, lfabp expression, and iron stores. In addition, a negative correlation was found between ppar expression, TBARS, carbonyl protein, and iron stores. In conclusion, our results suggest that the increase observed in the transport of lipids in the bloodstream and the decreased fatty acid oxidation in rats, which was promoted by iron dextran, might be attributed to increased oxidative stress

Glyphosate and Aminomethylphosphonic Acid (AMPA) Modulate Glutathione S-Transferase in Non-Tumorigenic Prostate Cells

Glyphosate (GLY) was developed in the early 1970s and has become the most used broad-spectrum herbicide in the world so far. Its main metabolite is aminomethylphosphonic acid (AMPA), and the accumulation of GLY and its derivative compounds raises some concerns regarding possible health outcomes. In this study, we aimed to evaluate the effects of GLY and AMPA on prostate cell lines by evaluating cell viability, proliferation, gene and protein expression, and cellular pathways involved in the response to oxidative stress. Our results indicated that GLY and AMPA reduced the cell viability of tumorigenic and non-tumorigenic prostate cell lines only at higher concentrations (10 mM GLY and 20 mM AMPA). In contrast, both compounds increased the clonogenicity of non-tumorigenic PNT2 cells, mainly at concentrations below the IC50 (5 mM GLY and 10 mM AMPA). Moreover, treatment of non-tumorigenic cells with low concentrations of GLY or AMPA for 48 h increased GSTM3 expression at both mRNA and protein levels. In contrast, the treatments decrease the GST activity and induced an increase in oxidative stress, mainly at lower concentrations. Therefore, both compounds can cause cellular damage even at lower concentrations in non-tumorigenic PNT2 cells, mainly affecting cell proliferation and oxidative stress

Dieta hipercolesterolemiante induz esteatose hepática e alterações na expressão de mRNA da NADPH oxidase em fígados de ratos.

Objetivo: Determinar se uma dieta hipercolesterolemiante induz esteatose hepatica, alterações na expressão de mRNA da NADPH oxidase e nas defesas antioxidantes. Materiais e métodos: Ratas Fischer foram divididas em dois grupos de oito animais de acordo com o tratamento recebido, controle (C) e hipercolesterolemico (H). Aquelas do grupo C foram alimentadas com dieta padrão (AIN-93M) e as do grupo H foram alimentadas com dieta hipercolesterolemiante (25% de óleo de soja e 1% de colesterol). As dietas foram oferecidas por oito semanas. Resultados: O grupo H apresentou acumulo de lipídios no fígado, aumento das atividades de ALT e AST e da concentração de colesterol no soro comparado ao grupo C. O marcador da peroxidacão lipídica (TBARS) e os níveis de mRNA das subunidades p47phox da NADPH-oxidase e p22phox foram aumentados no fígado de animais do grupo H, alem de alteração da atividade e expressão de enzimas antioxidantes. Conclusão: Os resultados mostram um aumento na expressão de subunidades da NADPH oxidase e alterações na atividade das enzimas antioxidantes na esteatose hepática induzida por dieta hipercolesterolemiante.Objective: This study aimed to determine whether a hypercholesterolemic diet induces hepatic steatosis, alterations in mRNA expression of NADPH oxidase subunits, and antioxidant defenses. Materials and methods: Fischer rats were divided into two groups of eight animals according to the treatment, control (C) and hypercholesterolemic diet (H). Those in group C were fed a standard diet (AIN-93M), and those of the group H were fed a hypercholesterolemic diet (25% soybean oil and 1% cholesterol). Results: The hypercholesterolemic diet did not affect body weight, but resulted in the accumulation of lipids in the liver, increased serum activities of aminotransferases and cholesterol levels. Biomarker of lipid peroxidation (TBARS) and mRNA expression of NADPH oxidase subunits p22phox and p47phox were increased in the liver of animals in group H. Besides, the activity and expression of antioxidant enzymes were altered. Conclusion: The results show increased mRNA expression of NADPH oxidase subunits and changes in antioxidant enzyme activities in diet-induced hepatic steatosis

Carqueja (Baccharis trimera) Protects against Oxidative Stress and β-Amyloid-Induced Toxicity in Caenorhabditis elegans

Carqueja (Baccharis trimera) is a native plant found throughout South America. Several studies have shown that Carqueja has antioxidant activity in vitro, as well as anti-inflammatory, antidiabetic, analgesic, antihepatotoxic, and antimutagenic properties. However, studies regarding its antioxidant potential in vivo are limited. In this study, we used Caenorhabditis elegans as a model to examine the antioxidant effects of a Carqueja hydroalcoholic extract (CHE) on stress resistance and lifespan and to investigate whether CHE has a protective effect in a C. elegans model for Alzheimer's disease. Here, we show for the first time, using in vivo assays, that CHE treatment improved oxidative stress resistance by increasing survival rate and by reducing ROS levels under oxidative stress conditions independently of the stress-related signaling pathways (p38, JNK, and ERK) and transcription factors (SKN-1/Nrf and DAF-16/Foxo) tested here. CHE treatment also increased the defenses against β-amyloid toxicity in C. elegans, in part by increasing proteasome activity and the expression of two heat shock protein genes. Our findings suggest a potential neuroprotective use for Carqueja, supporting the idea that dietary antioxidants are a promising approach to boost the defensive systems against stress and neurodegeneration

Oxidative stress in Mayaro virus infection.

Mayaro virus (MAYV) is a neglected tropical arbovirus that causes a febrile syndrome that is sometimes accompanied by incapacitating arthritis/arthralgia. The pathogenesis of MAYV has not been completely defined and oxidative stress mediated by an increase in reactive oxygen species (ROS) and/or depletion of antioxidant defences has been found to contribute to several aspects of viral disease. To investigate whether MAYV induced oxidative stress in host cells, we monitored ROS production, oxidative stress markers and antioxidant defences at different time points after infection. Our results show that MAYV induced significant oxidative stress in infected HepG2 cells, as indicated by the increase of malondialdehyde (MDA) and protein carbonyl levels, and by a significant decrease of the reduced versus oxidized glutathione (GSH/GSSG) ratio. Generally, MAYV-infected HepG2 cells also showed an increase in antioxidant defences. We observed an increase in the superoxide dismutase (SOD) and catalase (CAT) activities and the total glutathione content. To determine whether similar effects occurred in other cell types, we evaluated the ROS, MDA and SOD activity levels in J774 cells after MAYV infection. Similar to our observations in HepG2 cells, the J774 cells showed an increase in ROS, MDA and total SOD activity following MAYV infection. Thus, since the cellular redox environment is influenced by the production and removal of ROS, we hypothesize that the overproduction of ROS was responsible for the oxidative stress in response to the MAYV infection despite the increase in the antioxidant status. This study is the first report on the involvement of oxidative stress during MAYV infection. Collectively, our data shed light on some mechanisms that are operational in host cells following exposure to MAYV

High dietary salt decreases antioxidant defenses in the liver of fructose-fed insulin-resistant rats.

In this study we investigated the hypothesis that a high-salt diet to hyperinsulinemic rats might impair antioxidant defense owing to its involvement in the activation of sodium reabsorption to lead to higher oxidative stress. Rats were fed a standard (CON), a high-salt (HS), or a high-fructose (HF) diet for 10 weeks after which, 50% of the animals belonging to the HF group were switched to a regimen of high-fructose and high-salt diet (HFS) for 10 more weeks, while the other groups were fed with their respective diets. Animals were then euthanized and their blood and liver were examined. Fasting plasma glucose was found to be significantly higher (approximately 50%) in fructose-fed rats than in the control and HS rats, whereas fat liver also differed in these animals, producing steatosis. Feeding fructose-fed rats with the high-salt diet triggered hyperinsulinemia and lowered insulin sensitivity, which led to increased levels of serum sodium compared to the HS group. This resulted in membrane perturbation, which in the presence of steatosis potentially enhanced hepatic lipid peroxidation, thereby decreasing the level of antioxidant defenses, as shown by GSH/GSSG ratio (HFS rats, 7.098±2.1 versus CON rats, 13.2±6.1) and superoxide dismutase (HFS rats, 2.1±0.05 versus CON rats, 2.3±0.1%), and catalase (HFS rats, 526.6±88.6 versus CON rats, 745.8±228.7 U/mg ptn) activities. Our results indicate that consumption of a salt-rich diet by insulin-resistant rats may lead to regulation of sodium reabsorption, worsening hepatic lipid peroxidation associated with impaired antioxidant defenses