Effects of açai on oxidative stress, ER stress, and inflammation-related parameters in mice with high fat diet-fed induced NAFLD.

Non-alcoholic fatty liver disease (NAFLD), the most predominant liver disease worldwide, is a progressive condition that encompasses a spectrum of disorders ranging from steatosis to steatohepatitis, and, ultimately, cirrhosis and hepatocellular carcinoma. Although the underlying mechanism is complex and multifactorial, several intracellular events leading to its progression have been identified, including oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, and altered endoplasmic reticulum (ER) homeostasis. Phenolic compounds, such as those present in açai (Euterpe oleracea Mart.), are considered promising therapeutic agents due to their possible beneficial effects on the prevention and treatment of NAFLD. We tested in vitro effects of aqueous açai extract (AAE) in HepG2 cells and its influence on oxidative stress, endoplasmic reticulum stress, and inflammation in a murine model of high fat diet-induced NAFLD. In vitro AAE exhibited high antioxidant capacity, high potential to inhibit reactive oxygen species production, and no cytotoxicity. In vivo, AAE administration (3 g/kg) for six weeks attenuated liver damage (alanine aminotransferase levels), inflammatory process (number of inflammatory cells and serum TNFα), and oxidative stress, through the reduction of lipid peroxidation and carbonylation of proteins determined by OxyBlot and modulation of the antioxidant enzymes: glutathione reductase, SOD and catalase. No change was observed in collagen content indicating an absence of fibrosis, stress-related genes in RE, and protein expression of caspase-3, a marker of apoptosis. With these results, we provide evidence that açai exhibits hepatoprotective effects and may prevent the progression of liver damage related to NAFLD by targeting pathways involved in its progression.

Physical exercise improves body weight gain and liver function in malnourished rats without disturbing the redox balance / O exercício físico melhora o ganho de peso corporal e a função hepática em ratos desnutridos sem perturbar o balanço de redox

ABSTRACT Objective To study the relationship between exercise and malnourishment because recent evidence suggests that exercise can cause the beneficial adaptation of antioxidant systems, whereas malnourishment can cause harmful adaptation of these systems. Methods Thirty-two female Fischer rats were equally divided into Sedentary Control, Trained Control, Sedentary Malnourished and Trained Malnourished groups. The training protocol consisted of swimming for 30 minutes continuously for 5 days/week for 8 weeks. Results It was demonstrated that aspartate aminotransferase and alanine aminotransferase activities increased in malnourished rats, but physical training reversed these effects by lowering the raised levels. The glutathione level was diminished by malnourishment whereas physical training increased the levels of liver carbonyl protein and increased the levels of thiobarbituric acid reactive substances that were diminished by malnourishment. In addition, Trained Malnourished rats had a higher average body weight than Sedentary Malnourished ones (62.77g vs. 55.08g, respectively). Conclusion The data show that exercise was able to reverse or reduce damage caused by malnourishment, such as weight loss and liver dysfunction by a pathway independent of the participation of enzymes involved in antioxidant defense and that there is no interaction between exercise and malnutrition.

RESUMO Objetivo Estudar a relação entre exercício e desnutrição, pois evidências recentes sugerem que o exercício físico pode causar a adaptação benéfica de sistemas antioxidantes, enquanto a desnutrição pode causar adaptação prejudicial a esses sistemas. Métodos Trinta e duas ratas Fischer foram igualmente divididas nos grupos Controle Sedentário, Controle Treinado, Desnutrido Sedentário e Desnutrido Treinado. O protocolo de treinamento consistiu em nadar por 30 minutos continuamente por 5 dias/semana por 8 semanas. Resultados Demonstramos que as atividades de aspartato aminotransferase e alanina aminotransferase aumentaram em ratos desnutridos, mas o treinamento físico reverteu esses efeitos. O nível de glutationa foi diminuído pela desnutrição, enquanto o treinamento físico aumentou os níveis de proteína carbonilada do fígado e aumentou os níveis de substâncias reativas ao ácido tiobarbitúrico que foram diminuídas pela desnutrição. Além disso, os ratos desnutridos treinados tiveram um peso corporal médio maior que os desnutridos sedentários (62,77g vs 55,08g, respectivamente). Conclusão Os dados mostram que o exercício foi capaz de reverter ou reduzir os danos causados pela desnutrição, como perda de peso e a disfunção hepática por uma via independente da participação de enzimas envolvidas na defesa antioxidante e que não há interação entre exercício e desnutrição.

Biodegradable seeds of holmium don't change neurological function after implant in brain of rats.

AIM: To evaluate the surgical procedure and parenchymal abnormalities related to implantation of ceramic seeds with holmium-165 in rats' brain. BACKGROUND: An effective method of cancer treatment is brachytherapy in which radioactive seeds are implanted in the tumor, generating a high local dose of ionizing radiation that can eliminate tumor cells while protecting the surrounding healthy tissue. Biodegradable Ho166-ceramic-seeds have been addressed recently. METHODS AND MATERIALS: The experiments in this study were approved by the Ethics Committee on Animal Use at the Federal University of Ouro Preto, protocol number 2012/034. Twenty-one adult Fischer rats were divided into Naive Group, Sham Group and Group for seed implants (ISH). Surgical procedures for implantation of biodegradable seeds were done and 30 days after the implant radiographic examination and biopsy of the brain were performed. Neurological assays were also accomplished to exclude any injury resulting from either surgery or implantation of the seeds. RESULTS: Radiographic examination confirmed the location of the seeds in the brain. Neurological assays showed animals with regular spontaneous activity. The histological analysis showed an increase of inflammatory cells in the brain of the ISH group. Electron microscopy evidenced cytoplasmic organelles to be unchanged. Biochemical analyzes indicate there was neither oxidative stress nor oxidative damage in the ISH brain. CAT activity showed no difference between the groups as well as lipid peroxidation measured by TBARS. CONCLUSIONS: The analysis of the data pointed out that the performed procedure is safe as no animal showed alterations of the neurological parameters and the seeds did not promote histological architectural changes in the brain tissue.

Changes in cardiovascular responses to chemoreflex activation of rats recovered from protein restriction are not related to AT1 receptors.

NEW FINDINGS: What is the central question of this study? In this study, we sought to investigate whether cardiovascular responses to peripheral chemoreflex activation of rats recovered from protein restriction are related to activation of AT1 receptors. What is the main finding and its importance? This study highlights the fact that angiotensinergic mechanisms activated by AT1 receptors do not support increased responses to peripheral chemoreflex activation by KCN in rats recovered from protein restriction. Also, we found that protein restriction led to increased resting ventilation in adult rats, even after recovery. The effects of a low-protein diet followed by recovery on cardiorespiratory responses to peripheral chemoreflex activation were tested before and after systemic angiotensin II type 1 (AT1 ) receptor antagonism. Male Fischer rats were divided into control and recovered (R-PR) groups after weaning. The R-PR rats were fed a low-protein (8%) diet for 35 days and recovered with a normal protein (20%) diet for 70 days. Control rats received a normal protein diet for 105 days (CG105 ). After cannulation surgery, mean arterial pressure, heart rate, respiratory frequency, tidal volume and minute ventilation were acquired using a digital recording system in freely moving rats. The role of angintensin II was evaluated by systemic antagonism of AT1 receptors with losartan (20 mg kg-1 i.v.). The peripheral chemoreflex was elicited by increasing doses of KCN (20-160 µg kg min-1 , i.v.). At baseline, R-PR rats presented increased heart rate and minute ventilation (372 ± 34 beats min-1 and 1.274 ± 377 ml kg-1  min-1 ) compared with CG105 animals (332 ± 22 beats min-1 and 856 ± 112 ml kg-1  min-1 ). Mean arterial pressure was not different between the groups. Pressor and bradycardic responses evoked by KCN (60 µg kg-1 ) were increased in R-PR (+45 ± 13 mmHg and -77 ± 47 beats min-1 ) compared with CG105 rats (+25 ± 17 mmHg and -27 ± 28 beats min-1 ), but no difference was found in the tachypnoeic response. These differences were preserved after losartan. The data suggest that angiotensin II acting on AT1 receptors may not be associated with the increased heart rate, increased minute ventilation and acute cardiovascular responses to peripheral chemoreflex activation in rats that underwent postweaning protein restriction followed by recovery.

Açai (Euterpe oleracea Mart.) Upregulates Paraoxonase 1 Gene Expression and Activity with Concomitant Reduction of Hepatic Steatosis in High-Fat Diet-Fed Rats.

Açai (Euterpe oleracea Mart.), a fruit from the Amazon region, has emerged as a promising source of polyphenols. Açai consumption has been increasing owing to ascribed health benefits and antioxidant properties; however, its effects on hepatic injury are limited. In this study, we evaluated the antioxidant effect of filtered açai pulp on the expression of paraoxonase (PON) isoforms and PON1 activity in rats with nonalcoholic fatty liver disease (NAFLD). The rats were fed a standard AIN-93M (control) diet or a high-fat (HF) diet containing 25% soy oil and 1% cholesterol with or without açai pulp (2 g/day) for 6 weeks. Our results show that açai pulp prevented low-density lipoprotein (LDL) oxidation, increased serum and hepatic PON1 activity, and upregulated the expression of PON1 and ApoA-I in the liver. In HF diet-fed rats, treatment with açai pulp attenuated liver damage, reducing fat infiltration and triglyceride (TG) content. In rats receiving açai, increased serum PON1 activity was correlated with a reduction in hepatic steatosis and hepatic injury. These findings suggest the use of açai as a potential therapy for liver injuries, supporting the idea that dietary antioxidants are a promising approach to enhance the defensive systems against oxidative stress.

Carqueja (Baccharis trimera) Protects against Oxidative Stress and ß-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 ß-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.

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 rats were divided into two groups: the standard group (S), which was fed the AIN-93M diet, 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 pparα, and its downstream gene cpt1a, which is involved in lipid oxidation. Iron dextran also increased mRNA levels of apoB-100, MTP, and L-FABP 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 pparα 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.

Protective effect of Baccharis trimera extract on acute hepatic injury in a model of inflammation induced by acetaminophen.

BACKGROUND: Acetaminophen (APAP) is a commonly used analgesic and antipyretic. When administered in high doses, APAP is a clinical problem in the US and Europe, often resulting in severe liver injury and potentially acute liver failure. Studies have demonstrated that antioxidants and anti-inflammatory agents effectively protect against the acute hepatotoxicity induced by APAP overdose. METHODS: The present study attempted to investigate the protective effect of B. trimera against APAP-induced hepatic damage in rats. The liver-function markers ALT and AST, biomarkers of oxidative stress, antioxidant parameters, and histopathological changes were examined. RESULTS: The pretreatment with B. trimera attenuated serum activities of ALT and AST that were enhanced by administration of APAP. Furthermore, pretreatment with the extract decreases the activity of the enzyme SOD and increases the activity of catalase and the concentration of total glutathione. Histopathological analysis confirmed the alleviation of liver damage and reduced lesions caused by APAP. CONCLUSIONS: The hepatoprotective action of B. trimera extract may rely on its effect on reducing the oxidative stress caused by APAP-induced hepatic damage in a rat model. General Significance. These results make the extract of B. trimera a potential candidate drug capable of protecting the liver against damage caused by APAP overdose.

Caraparu virus induces damage and alterations in antioxidant defenses in the liver of BALB/c mice after subcutaneous infection.

Oxidative stress is a disturbance in the oxidant-antioxidant balance leading to potential cellular damage. Most cells can tolerate a mild degree of oxidative stress because they have a system that counteracts oxidation that includes antioxidant molecules such as glutathione (GSH) and superoxide dismutase (SOD). Disruption of the host antioxidant status has been recognized as an important contributor to the pathogenesis of many viruses. Caraparu virus (CARV) is a member of group C of the Bunyaviridae family of viruses. In South American countries, group C bunyaviruses are among the common agents of human febrile illness and have caused multiple notable outbreaks of human disease in recent decades; nevertheless, little is known about the pathogenic characteristics of these viruses. The purpose of this study was to examine the hepatic pathogenesis of CARV in mice and the involvement of oxidative stress and antioxidant defenses on this pathology. Following subcutaneous infection of BALB/c mice, CARV was detected in the liver, and histopathology revealed acute hepatitis. Increased serum levels of aspartate and alanine aminotransferases (AST/ALT) and greater hepatic expression of the proinflammatory cytokine tumor necrosis factor-α (TNF-α) were found in infected animals. CARV infection did not alter the biomarkers of oxidative stress but caused an increase in GSH content and altered the expression and activity of SOD. This is the first report of an alteration of oxidative homeostasis upon CARV infection, which may, in part, explain the hepatic pathogenesis of this virus, as well as the pathogenesis of other Bunyaviridae members.

Hypercholesterolemic diet induces hepatic steatosis and alterations in mRNA expression of NADPH oxidase in rat livers.

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 p22(phox) and p47(phox) 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.

Hypercholesterolemic diet induces hepatic steatosis and alterations in mRNA expression of NADPH oxidase in rat livers / Dieta hipercolesterolemiante induz esteatose hepática e alterações na expressão de mRNA da NADPH oxidase em fígados de ratos

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. Arq Bras Endocrinol Metab. 2014;58(3):251-9.

Objetivo Determinar se uma dieta hipercolesterolemiante induz esteatose hepática, 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 hipercolesterolêmico (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 acúmulo 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 peroxidação lipídica (TBARS) e os níveis de mRNA das subunidades p47phox da NADPH-oxidase e p22phox foram aumentados no fígado de animais do grupo H, além 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. Arq Bras Endocrinol Metab. 2014;58(3):251-9.

Iron toxicity mediated by oxidative stress enhances tissue damage in an animal model of diabetes.

Although iron is a first-line pro-oxidant that modulates clinical manifestations of various systemic diseases, including diabetes, the individual tissue damage generated by active oxidant insults has not been demonstrated in current animal models of diabetes. We tested the hypothesis that oxidative stress is involved in the severity of the tissues injury when iron supplementation is administered in a model of type 1 diabetes. Streptozotocin (Stz)-induced diabetic and non-diabetic Fischer rats were maintained with or without a treatment consisting of iron dextran ip at 0.1 mL day(-1) doses administered for 4 days at intervals of 5 days. After 3 weeks, an extensive increase (p < 0.001) in the production of reactive oxygen species (ROS) in neutrophils of the diabetic animals on iron overload was observed. Histological analysis revealed that this treatment also resulted in higher (p < 0.05) tissue iron deposits, a higher (p < 0.001) number of inflammatory cells in the pancreas, and apparent cardiac fibrosis, as shown by an increase (p < 0.05) in type III collagen levels, which result in dysfunctional myocardial. Carbonyl protein modification, a marker of oxidative stress, was consistently higher (p < 0.01) in the tissues of the iron-treated rats with diabetes. Moreover, a significant positive correlation was found between ROS production and iron pancreas stores (r = 0.42, p < 0.04), iron heart stores (r = 0.54, p < 0.04), and change of the carbonyl protein content in pancreas (r = 0.49, p < 0.009), and heart (r = 0.48, p < 0.02). A negative correlation was still found between ROS production and total glutathione content in pancreas (r = -0.50, p < 0.03) and heart (r = -0.45, p < 0.04). In conclusion, our results suggest that amplified toxicity in pancreatic and cardiac tissues in rats with diabetes on iron overload might be attributed to increased oxidative stress.

Vildagliptin ameliorates oxidative stress and pancreatic beta cell destruction in type 1 diabetic rats.

BACKGROUND AND AIMS: It is believed that oxidative stress plays a role in the pathogenesis of diabetes mellitus. Several strategies have been developed with the objective of minimizing diabetic complications. Among these, inhibitors of dipeptidyl peptidase-IV (DPP-IV), which act by blocking degradation of incretin hormones, glucagon-like peptide hormone (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), have been the focus of many studies. It is known that, among the effects of incretins, we highlight its insulinotropic and cytoprotective effects on pancreatic ß-cells. The objective of this study was to evaluate the possible protective effects of treatment with vildagliptin, a DPP-IV inhibitor, in ß-cells in an experimental model of type 1 diabetes induced by streptozotocin (STZ). METHODS: Rats were treated for 4 weeks with vildagliptin at concentrations of 5 and 10 mg/kg. In order to observe the pancreatic damage and the possible protective effects of vildagliptin treatment, we measured stress markers TBARS and protein carbonyl, antioxidant enzymes SOD and catalase, and analyzed pancreatic histology. RESULTS: The treatment was effective in modulating stress in pancreatic tissue, both by reducing levels of stress markers as well as by increasing activity of SOD and catalase. After analyzing the pancreatic histology, we found that vildagliptin was also able to preserve islets and pancreatic ß-cells, especially at the concentration of 5 mg/kg. CONCLUSION: Thus, our results suggest that vildagliptin ameliorates oxidative stress and pancreatic beta cell destruction in type 1 diabetic rats. However, to evaluate the real potential of this medication in type 1 diabetes, further studies are needed.

Whey protein improves HDL/non-HDL ratio and body weight gain in rats subjected to the resistance exercise

The aim of this study was to evaluate the effects of resistance exercise, such as weight-lifting (WL) on the biochemical parameters of lipid metabolism and cardiovascular disease risk in the rats fed casein (control) or whey protein (WP) diets. Thirty-two male Fisher rats were randomly assigned to sedentary or exercise-trained groups and were fed control or WP diets. The WL program consisted of inducing the animals to perform the sets of jumps with weights attached to the chest. After seven weeks, arteriovenous blood samples were collected for analysis. The WL or WP ingestion were able to improve the lipid profile, reducing the TC and non-HDL cholesterol concentrations, but only WP treatment significantly increased the serum HDL concentrations, thereby also affecting the TC/HDL and HDL/non-HDL ratios. However, WL plus WP was more effective in improving the HDL/non-HDL ratio than the exercise or WP ingestion alone and the body weight gain than exercise without WP ingestion.

Iron overload potentiates diet-induced hypercholesterolemia and reduces liver PPAR-α expression in hamsters.

Iron stores and lipids are related to the development of cardiovascular disease. Given that peroxisome proliferator-activated receptor alpha (PPAR-α) regulates important physiological processes that impact lipid and glucose homeostasis, we decided to investigate the effects of iron overload on serum lipids and the liver expression of PPAR-α, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and cholesterol 7α-hydroxylase. Hamsters were divided into four groups. The standard group (S) was fed the AIN-93M diet, the SI group was fed the diet and iron injections, the hypercholesterolemic group (H) was fed a standard diet containing cholesterol, and the HI group was fed a high-cholesterol diet and iron injections. Serum cholesterol in the HI group was higher than in the H group. Gene expression analysis of PPAR-α showed that the HI group had a lower PPAR-α expression than H. These data show that iron, when associated with a high-fat diet, can cause increased serum cholesterol levels, possibly due to a reduction in PPAR-α expression.

Differential expression of iron metabolism proteins in diabetic and diabetic iron-supplemented rat liver.

Diabetes mellitus is associated with altered iron homeostasis that can potentially effect reactive oxygen species generation and contribute to diabetes-related complications. We investigated, by quantitative polymerase chain reaction, whether the expression of liver hepcidin, ferritin, and TfR-1 is altered in diabetes. Rats in the control (C) group received a standard diet; control iron (CI) group received a standard diet supplemented with iron; diabetic (D) group received an injection of streptozotocin; and diabetic iron (DI) group received streptozotocin and the diet with iron. Animals of the D group showed higher levels of serum iron, increased concentration of carbonyl protein, and a decrease in antioxidant status. Group D rats showed increased hepatic expression of Trf-1 compared to the other groups. Iron supplementation reversed this increase. Hepcidin mRNA was 81% higher in DI than in C and CI rats. The results suggest that diabetes, with or without excess iron, can cause perturbations in iron status, hepcidin and Trf-1 expression.

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.

Effects of the interaction of diabetes and iron supplementation on hepatic and pancreatic tissues, oxidative stress markers, and liver peroxisome proliferator-activated receptor-α expression.

This study evaluated the effects of the interaction of diabetes and a carbonyl iron supplemented on hepatic and pancreatic tissues, oxidative stress markers and liver peroxisome proliferator-activated receptor-α expressions. Hamsters were divided: Control which received a standard AIN 93 diet; Control Iron, composed of control animals that received a diet with 0.83% carbonyl iron; Diabetic, composed of animals that received a injection of streptozotocin (50 mg/kg, intraperitoneal) on day 35; and Diabetic Iron composed of streptozotocin treated animals that received a diet supplemented with carbonyl iron. Diabetes increased the glucose level and reduced triglycerides. Diabetic Iron group showed higher levels of glucose and serum triglycerides as compared to the Diabetic group. Diabetes decreased mRNA levels of peroxisome proliferator-activated receptor-α. Iron attenuated the diabetes induced down regulation of peroxisome proliferator-activated receptor-α mRNA. Moreover, diabetes increased carbonyl protein and decreased glutathione levels and catalase activity, while iron attenuated the increase in levels of carbonyl protein and attenuated the decrease in those of glutathione level and catalase activity. Histological analysis shows that supplementation iron caused an increase in the size of the islets in Control Iron. The results show that iron does not aggravated liver oxidant/antioxidant status and peroxisome proliferator-activated receptor-α expression in diabetic hamsters.

Açaí (Euterpe oleraceae Martius): composição química e bioatividades / Açaí (Euterpe oleraceae Martius): chemical composition and bioactivity

Açaí (Euterpe oleraceae Martius) is a typically Brazilian fruit and itis economically important. Popular reports indicate the medicinal use of its juice and articles which describe its chemical composition have demonstrated the presence of phenolic compounds, fibers, unsaturated fatty acids and phytosterols, suggesting its potential as a functional food. The present article aims at presenting a review about the fruit, stressing its chemical compounds and their bioactivity in vitro and in vivo. The focus on açaí is based on the fruit large consumption both in the internal market and abroad, and also on the investigations which have assessedits functional properties. The results of these investigations have shown that the fruit exhibits a high antioxidant capacity, anti-inflammatory properties and a hypocholesterolemic effect. Given these properties and health claims assigned to açaí, the study and consumption of this fruit should be encouraged.

Açaí (Euterpe oleraceae Martius) es una fruta típica de Brasil y económicamente importante. Informes populares indican el uso medicinal de su jugo y los trabajos que describen su composición química muestran la presenciade compuestos fenólicos, fibra, ácidos grasos insaturados y fitoesteroles, lo que sugiere su potencial como alimento funcional. Este trabajo tiene como objetivo presentar una revisión sobre açaí, haciendo hincapié en sus componentes químicos y sus bioactividadin vitro e in vivo. El interés en el açaí se basa en el consumo generalizado de este producto tanto a nivel nacional como fuera del país y también en las investigaciones que evalúan sus propiedades funcionales. Los resultados de las investigaciones muestran que el fruto presenta elevada capacidad antioxidante, propiedad antiinflamatoria y efecto hipocolesterolémico. Considerando estas propiedades y las alegaciones saludables del consumo de açaí, el estudio y el consumo de esta fruta debe ser estimulado.

O açaí (Euterpe oleraceae Martius) é um fruto tipicamente brasileiro e economicamente importante. Relatos populares indicam o uso medicinal do seu suco e trabalhos que descrevem sua composição química, demonstram a presença de compostos fenólicos, fibras, ácidos graxos insaturados e fitosteróis, sugerindo seu potencial como alimentofuncional. Este trabalho tem como objetivo apresentar uma revisão sobre o açaí, enfatizando os seus componentes químicos e suas bioatividades in vitro e in vivo. O enfoque no açaí fundamenta-se no amplo consumo deste fruto tanto no mercado interno quanto fora do país e também nas investigações que avaliam suas propriedades funcionais. Os resultados dessas investigações mostram que este fruto exibe alta capacidade antioxidante, propriedades anti-inflamatórias e efeito hipocolesterolêmico. Diante dessas propriedades e as alegações de saúde designadas ao açaí, o estudo e o consumo deste fruto devem ser estimulados.

Efeito da estreptozotocina sobre os perfis glicêmico e lipídico e o estresse oxidativo em hamsters / Effect of streptozotocin on the glycemic and lipid profiles and oxidative stress in hamsters

OBJETIVO: Este estudo avaliou os efeitos da estreptozotocina nos perfis glicêmico e lipídico e marcadores de estresse oxidativo em hamsteres. MATERIAIS E MÉTODOS: Hamsteres machos Golden Syrian foram divididos em dois grupos: grupo diabético (D), que recebeu uma única injeção de estreptozotocina (STZ - 50 mg/kg), e grupo controle (C), que recebeu injeção de tampão citrato. Os animais foram eutanasiados após 10 dias de experimento e o sangue, o fígado e rins foram coletados. RESULTADOS: O grupo diabético apresentou níveis maiores de glicose, triacilgliceróis e colesterol séricos e maior concentração de substâncias reativas ao ácido tiobarbitúrico (TBARs) no fígado e nos rins. Também apresentou significativo aumento da concentração de glutationa no fígado e menores atividades da paraoxonase e do superóxido dismutase. CONCLUSÃO: Hamsteres fornecem um bom modelo para o diabetes melito do tipo I e estresse oxidativo, similar ao da síndrome humana, e poderão ser adequados para a análise de compostos antidiabéticos.

OBJECTIVE: This study evaluated the effects of streptozotocin on glycemic and lipid profiles and oxidative stress status in hamsters. MATERIALS AND METHODS: Male Golden Syrian hamsters were divided in diabetic group (D) which received a streptozotocin single injection (STZ - 50 mg/kg), and control group (C) which received a single injection of the vehicle citrate buffer. Animals were euthanized after 10 days of experiment and blood, liver and kidneys were collected. RESULTS: The diabetic group had higher levels of glucose, triacylglycerols and cholesterol in serum and thiobarbituric acid reactive substances (TBARS) concentration increased in the liver and kidneys. Diabetes induced a significant increase in glutathione concentration in the liver and decreased paraoxonase and superoxide dismutase activities. CONCLUSION: Hamsters provide a novel animal model for diabetes mellitus and oxidative stress, similar to the human syndrome, which may be suitable for the testing of antidiabetic compounds.