The abundance of comammox bacteria was higher than that of ammonia-oxidizing archaea and bacteria in rhizosphere of emergent macrophytes in a typical shallow lake riparian / La abundancia de bacterias comammox fue mayor que la de arqueas y bacterias oxidantes de amoníaco en la rizosfera de macrófitos emergentes en un típico lago ribereño poco profundo

Complete ammonia oxidation (comammox) bacteria can complete the whole nitrification process independently, which not only challenges the classical two-step nitrification theory but also updates long-held perspective of microbial ecological relationship in nitrification process. Although comammox bacteria have been found in many ecosystems in recent years, there is still a lack of research on the comammox process in rhizosphere of emergent macrophytes in lakeshore zone. Sediment samples were collected in this study from rhizosphere, far-rhizosphere, and non-rhizosphere of emergent macrophytes along the shore of Lake Liangzi, a shallow lake. The diversity of comammox bacteria and amoA gene abundance of comammox bacteria, ammonia-oxidizing archaea (AOA), and ammonia-oxidizing bacteria (AOB) in these samples were measured. The results showed that comammox bacteria widely existed in the rhizosphere of emergent macrophytes and fell into clade A.1, clade A.2, and clade B, and clade A was the predominant community in all sampling sites. The abundance of comammox amoA gene (6.52 × 106–2.45 × 108 copies g−1 dry sediment) was higher than that of AOB amoA gene (6.58 × 104–3.58 × 106 copies g−1 dry sediment), and four orders of magnitude higher than that of AOA amoA gene (7.24 × 102–6.89 × 103 copies g−1 dry sediment), suggesting that the rhizosphere of emergent macrophytes is more favorable for the growth of comammox bacteria than that of AOB and AOA. Our study indicated that the comammox bacteria may play important roles in ammonia-oxidizing processes in all different rhizosphere regions.(AU)

Effect of hypobaric hypoxia on the fiber type transition of skeletal muscle: a synergistic therapy of exercise preconditioning with a nanocurcumin formulation

Hypobaric hypoxia (HH) leads to various adverse effects on skeletal muscles, including atrophy and reduced oxidative work capacity. However, the effects of HH on muscle fatigue resistance and myofiber remodeling are largely unexplored. Therefore, the present study aimed to explore the impact of HH on slow-oxidative fibers and to evaluate the ameliorative potential of exercise preconditioning and nanocurcumin formulation on muscle anti-fatigue ability. C2C12 cells (murine myoblasts) were used to assess the effect of hypoxia (0.5%, 24 h) with and without the nanocurcumin formulation (NCF) on myofiber phenotypic conversion. To further validate this hypothesis, male Sprague Dawley rats were exposed to a simulated HH (7620 m) for 7 days, along with NCF administration and/or exercise training. Both in vitro and in vivo studies revealed a significant reduction in slow-oxidative fibers (p < 0.01, 61% vs. normoxia control) under hypoxia. There was also a marked decrease in exhaustion time (p < 0.01, 65% vs. normoxia) in hypoxia control rats, indicating a reduced work capacity. Exercise preconditioning along with NCF supplementation significantly increased the slow-oxidative fiber proportion and exhaustion time while maintaining mitochondrial homeostasis. These findings suggest that HH leads to an increased transition of slow-oxidative fibers to fast glycolytic fibers and increased muscular fatigue. Administration of NCF in combination with exercise preconditioning restored this myofiber remodeling and improved muscle anti-fatigue ability. (AU)

Especies reactivas de oxígeno: papel en la función vascular y en la disfunción endotelial asociada a la enfermedad metabólica / Reactive oxygen species: role in vascular function and in metabolic disease-associated endothelial dysfunction

El estrés oxidativo, alteración de la homeostasis REDOX en células y tejidos con un incremento de los niveles de especies reactivas de oxígeno (ROS), es un mecanismo patogénico común a múltiples patologías como las enfermedades cardiovasculares, los desórdenes neurodegenerativos, la inflamación y el cáncer, razón por la cual ha existido una investigación intensa en las últimas décadas sobre los posibles efectos protectores de las terapias antioxidantes en estas enfermedades. No obstante, la señalización REDOX juega, por otra parte, un papel crítico en la homeostasis y supervivencia celular, y las ROS son producidas en pequeñas cantidades durante la función celular normal. Las investigaciones llevadas a cabo en nuestro grupo han estado enfocadas al estudio del estrés oxidativo como factor patogénico clave en la disfunción endotelial en la obesidad y en otros estados de resistencia a la insulina. La disfunción endotelial subyace a las complicaciones vasculares de la diabetes y la obesidad, y representa un fenotipo endotelial mal adaptado con alteración de la función vasodilatadora, angiogénica y de barrera del endotelio, lo que conduce a un estado vasoconstrictor, proinflamatorio y protrombótico de la pared vascular. Debido a su capacidad de inhabilitar el óxido nítrico (NO), las ROS son en parte responsables de la disfunción endotelial. Por otra parte, nuestros estudios durante estos años han permitido caracterizar el papel clave de ROS como el H2O2 en la función endotelial de arterias de resistencia renales y coronarias, y su participación en la función vascular mediante la modulación de canales iónicos y enzimas implicados en vías de señalización de la pared arterial. Estas investigaciones sugieren la necesidad de valorar el papel de las ROS en los procesos fisiológicos de los distintos lechos vasculares y de revisar los esfuerzos en la búsqueda de terapias antioxidantes para las complicaciones vasculares de estados de resistencia a la insulina teniendo en cuenta la implicación de las ROS en la función endotelial normal. Palabras clave: especies reactivas de oxígeno (ROS), endotelio vascular, hiperpolarización derivada del endotelio (EDH), estrés oxidativo, obesidad, disfunción endotelial

Oxidative stress, impairment of REDOX homeostasis in cells and tissues leading to increased levels of reactive oxygen species (ROS), is a pathogenic mechanism underlying numerous pathologies including cardiovascular diseases, cancer, neurodegenerative disorders and inflammation. Therefore, there has been an intensive investigation during the last decades on the potential protective effects of antioxidant therapies on these disorders. Nevertheless, REDOX signaling plays a critical role in homeostasis and cell survival, and ROS are produced in small amount during normal cell function. Investigations carried out in our group during the last decade have been focused on the study of oxidative stress as a key pathogenic factor in endothelial and vascular dysfunction of resistance arteries in obesity and other insulin resistant states. Endothelial dysfunction underlies vascular complications of diabetes and obesity, and represents a maladapted endothelial phenotype consisting of impaired vasodilatation, angiogenesis and barrier function leading to a vasoconstrictor, pro-inflammatory and pro-thrombotic state of the vascular wall. ROS are involvedin endothelial dysfunction since they reduce bioavailability of nitric oxide (NO). On the other hand, our investigations have provided evidence for a key role of ROS such as hydrogen peroxide (H2O2) in the endothelial function of healthy coronary and renal resistance arteries, and its involvement in vascular function through modulation of ion channels and enzymes involved in signalling pathways of the arterial wall.These investigations suggest the need to assess the functional role of ROS in the different vascular beds and to revise the efforts in the search of antioxidant therapies for vascular complications of metabolic diseases by taking into account ROS involvement in endothelial function

Role of the antioxidant defense system during the production of lignocellulolytic enzymes by fungi

Fungi are used for the production of several compounds and the efficiency of biotechnological processes is directly related to the metabolic activity of these microorganisms. The reactions catalyzed by lignocellulolytic enzymes are oxidative and generate reactive oxygen species (ROS). Excess of ROS can cause serious damages to cells, including cell death. Thus, the objective of this work was to evaluate the lignocellulolytic enzymes produced by Pleurotus sajor-caju CCB020, Phanerochaete chrysosporium ATCC 28326, Trichoderma reesei RUT-C30, and Aspergillus niger IZ-9 grown in sugarcane bagasse and two yeast extract (YE) concentrations and characterize the antioxidant defense system of fungal cells by the activities of superoxide dismutase (SOD) and catalase (CAT). Pleurotus sajor-caju exhibited the highest activities of laccase and peroxidase in sugarcane bagasse with 2.6 g of YE and an increased activity of manganese peroxidase in sugarcane bagasse with 1.3 g of YE was observed. However, P. chrysosporium showed the highest activities of exoglucanase and endoglucanase in sugarcane bagasse with 1.3 g of YE. Lipid peroxidation and variations in SOD and CAT activities were observed during the production of lignocellulolytic enzymes and depending on the YE concentrations. The antioxidant defense system was induced in response to the oxidative stress caused by imbalances between the production and the detoxification of ROS

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Cyanobacterial extract-mediated synthesis of silver nanoparticles and their application in ammonia sensing

Green route for silver nanoparticle synthesis has gained increasing attention. Cyanobacteria are one of the promising organisms to produce a number of secondary metabolites that are capable of reducing silver ions to small-sized silver nanoparticles. In the present study, we employed an aqueous extract of the cyanobacterium Haloleptolyngbya alcalis KR2005/106 isolated from a soda lake for biosynthesis of silver nanoparticles (AgNPs). The extract acted as a reducing agent for AgNPs synthesis and resulted formation of nanoparticles <50 nm in size. In this study, synthesis of AgNPs obtained only in the sample exposed to photosynthetically active radiation (PAR) while the synthesis of AgNPs was not observed in the samples kept in dark. The biogenic fabrication of AgNPs was carried out by optimizing several governing parameters such as concentration of the silver nitrate solution, pH, temperature, and amount of biomass. Results obtained through different analytical techniques revealed that cyanobacterial taxon H. alcalis isolated from saline-alkaline habitat is a potential candidate for biosynthesis of optimum-sized spherical AgNPs. Surface plasmon resonance (SPR) property of AgNPs was exploited for aqueous ammonia sensing and revealed that AgNPs synthesized using aqueous extract of cyanobacterium H. alcalis could be employed for colorimetric detection of dissolved ammonia for monitoring quality of water

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Reduction-oxidation (redox) system in radiation-induced normal tissue injury: molecular mechanisms and implications in radiation therapeutics

Every year, millions of cancer patients undergo radiation therapy for treating and destroying abnormal cell growths within normal cell environmental conditions. Thus, ionizing radiation can have positive therapeutic effects on cancer cells as well as post-detrimental effects on surrounding normal tissues. Previous studies in the past years have proposed that the reduction and oxidation metabolism in cells changes in response to ionizing radiation and has a key role in radiation toxicity to normal tissue. Free radicals generated from ionizing radiation result in upregulation of cyclooxygenases (COXs), nitric oxide synthase (NOSs), lipoxygenases (LOXs) as well as nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), and their effected changes in mitochondrial functions are markedly noticeable. Each of these enzymes is diversely expressed in multiple cells, tissues and organs in a specific manner. Overproduction of reactive oxygen radicals (ROS), reactive hydroxyl radical (ROH) and reactive nitrogen radicals (RNS) in multiple cellular environments in the affected nucleus, cell membranes, cytosol and mitochondria, and other organelles, can specifically affect the sensitive and modifying enzymes of the redox system and repair proteins that play a pivotal role in both early and late effects of radiation. In recent years, ionizing radiation has been known to affect the redox functions and metabolism of NADPH oxidases (NOXs) as well as having destabilizing and detrimental effects on directly and indirectly affected cells, tissues and organs. More noteworthy, chronic free radical production may continue for years, increasing the risk of carcinogenesis and other oxidative stress-driven degenerative diseases as well as pathologies, in addition to late effect complications of organ fibrosis. Hence, knowledge about the mechanisms of chronic oxidative damage and injury in affected cells, tissues and organs following exposure to ionizing radiation may help in the development of treatment and management strategies of complications associated with radiotherapy (RT) or radiation accident victims. Thus, this medically relevant phenomenon may lead to the discovery of potential antioxidants and inhibitors with promising results in targeting and modulating the ROS/NO-sensitive enzymes in irradiated tissues and organ injury systems

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High fat diet and high polyphenols beverages effects in enzymatic and non-enzymatic antioxidant activity / Efectos de dieta con alto contenido de grasa y bebidas ricas en polifenoles en la actividad antioxidante enzimática y no enzimática

Background: High fat diets have been implicated in the generation of reactive oxygen species (ROS). Polyphenols from grapes may reduce ROS and restore oxidative balance. The aim of this study is to investigate the antioxidant properties of high polyphenols beverages associated with a high fat diet in enzymatic and non-enzymatic antioxidant activity. Material and methods: Fifty female rats were divided into five groups: a) control group (CG) - control diet (4% fat); b) high fat diet group (HFD) - high fat diet (20% fat); c) grape juice group (GJ) - grape juice (15 ml/day) + high fat diet; d) red wine group (RW) - red wine (10 ml/day) + high fat diet; and e) resveratrol solution group (RS) - resveratrol solution (15 ml/day) + high fat diet. Eight weeks later, the superoxide dismutase, catalase and glutathione peroxidase activities were measured. Superoxide dismutase activity was assayed by measuring the inhibition of adrenaline auto-oxidation, catalase by the decrease rate in hydrogen peroxide and glutathione peroxidase by monitoring the oxidation of nicotinamide adenine dinucleotide phosphate. Non-enzymatic antioxidant activity was assessed by oxygen radical absorbance capacity and DDPH (free radical sequestration 2,2-diphenyl-1-picryhydracil) method in the animal’s plasma. Results: GC and GJ presented the lowest glutathione peroxidase activity, pointing to a possible protective effect of grape juice against high levels of ROS (p < 0.05). RW increased catalase activity when compared to the RS (p <0 .05). Superoxide dismutase activity and non-enzymatic antioxidant plasma activity were similar in all groups. Conclusion: Grape juice showed to be the most effective in minimizing the deleterious effects of a high fat diet. Resveratrol did not present any benefit and red wine possibly shows a harmful effect due to ethanol content (AU)

Introducción: las dietas ricas en grasas se han implicado en la generación de especies reactivas del oxigeno (ROS). Los polifenoles de las uvas pueden reducir el ROS y restaurar el equilibrio oxidativo. El objetivo de este estudio es investigar las propiedades antioxidantes de las bebidas ricas en polifenoles asociadas con una dieta rica en grasa en la actividad antioxidante enzimática y no enzimática. Material y métodos: cincuenta ratas fueron divididas en cinco grupos: a) grupo control (CG) - dieta de control (4% de grasa); b) grupo rica en grasa (HFD) - dieta con 20% de grasa; c) jugo de uva (GJ) - jugo (15 ml/día) + dieta rica en grasas; d) vino tinto (RW) - vino tinto (10 ml/día) + dieta rica en grasas; y e) grupo solución de resveratrol (RS) - solución de resveratrol (15 ml/día) + dieta rica en grasas. Se midieron superoxido dismutasa, catalasa y glutation peroxidasa. La actividad de superoxido dismutasa para la inhibición de la auto-oxidación de adrenalina, la catalasa por la tasa de disminución de peróxido de hidrogeno y glutation peroxidasa monitorizando la oxidación de nicotinamida adenina dinucleotido fosfato. La actividad antioxidante no enzimatica se midió por el método de capacidad de absorción de radicales de oxígeno y DDPH (moléculas estables de radicales libres 2,2-difenil-1-picrihidrazilo). Resultados: GC y GJ presentaron la menor actividad de glutation peroxidasa, señalando un posible efecto protector del jugo de uva frente a altos niveles de ROS (p < 0,05). RW aumento la actividad de catalasa en comparación con RS (p < 0,05). Superoxido dismutasa y la actividad antioxidante no enzimatica fueron similares. Conclusiones: el jugo demostró ser el más eficaz para minimizar los efectos deletereos de una dieta rica en grasas. Resveratrol no presento ningún beneficio y el vino tinto posiblemente muestra un efecto perjudicial debido al contenido de etanol (AU)

Reducing mitochondrial bound hexokinase II mediates transition from non-injurious into injurious ischemia/reperfusion of the intact heart

Ischemia/reperfusion (I/R) of the heart becomes injurious when duration of the ischemic insult exceeds a certain threshold (approximately ≥20 min). Mitochondrial bound hexokinase II (mtHKII) protects against I/R injury, with the amount ofmtHKII correlating with injury. Here, we examine whether mtHKII can induce the transition from non-injurious to injurious I/R, by detaching HKII from mitochondria during a non-injurious I/R interva l . Additionally, we examine possible underlying mechanisms (increased reactive oxygen species (ROS), increased oxygen consumption (MVO2) and decreased cardiac energetics) associated with this transition. Langendorff perfused rat hearts were treated for 20 min with saline, TAT-only or 200 nM TAT-HKII, a peptide that translocates HKII from mitochondria. Then, hearts were exposed to non-injurious 15-min ischemia, followed by 30-min reperfusion. I/R injury was determined by necrosis (LDH release) and cardiac mechanical recovery. ROS were measured by DHE fluorescence. Changes in cardiac respiratory activity (cardiac MVO2 and efficiency and mitochondrial oxygen tension (mitoPO2) using protoporphyrin IX) and cardiac energetics (ATP, PCr, ΔGATP) were determined following peptide treatment.When exposed to 15-min ischemia, control hearts had no necrosis and 85% recovery of function. Conversely, TAT-HKII treatment resulted in significant LDH release and reduced cardiac recovery (25%), indicating injurious I/R. This was associated with increased ROS during ischemia and reperfusion. TAT-HKII treatment reducedMVO2 and improved energetics (increased PCr) before ischemia, without affecting MVO2/RPP ratio or mitoPO2. In conclusion, a reduction in mtHKII turns non-injurious I/R into injurious I/R. Loss of mtHKII was associated with increased ROS during ischemia and reperfusion, but not with increased MVO2 or decreased cardiac energetics before damage occurs

Diagnóstico y prevención de la cardiotoxicidad inducida por fármacos antineoplásicos: de la imagen a las tecnologías «ómicas» / Early diagnosis and prediction of anticancer drug-induced cardiotoxicity: from cardiac imaging to ‘omics’ technologies

La insuficiencia cardiaca secundaria al tratamiento del cáncer continúa siendo una causa significativa de morbilidad y mortalidad en el paciente oncológico. A menudo estos pacientes no tienen manifestaciones de la enfermedad hasta que la insuficiencia cardiaca se presenta. Sería necesario identificar de manera precisa qué individuos están en riesgo de cardiotoxicidad, incluso antes de las manifestaciones clínicas. El objetivo de este trabajo es ofrecer una revisión sobre el papel prometedor de las técnicas de imagen y las tecnologías «ómicas», especialmente la proteómica y la genómica, en la prevención y el diagnóstico precoz de la cardiotoxicidad, así como en la respuesta individual de cada paciente al tratamiento antineoplásico (AU)

Heart failure due to antineoplastic therapy remains a major cause of morbidity and mortality in oncological patients. These patients often have no prior manifestation of disease. There is therefore a need for accurate identification of individuals at risk of such events before the appearance of clinical manifestations. The present article aims to provide an overview of cardiac imaging as well as new ‘-omics’ technologies, especially with regard to genomics and proteomics as promising tools for the early detection and prediction of cardiotoxicity and individual responses to antineoplastic drugs (AU)

Electrochemical characterization of Geobacter lovleyi identifies limitations of microbial fuel cell performance in constructed wetlands

Power generation in microbial fuel cells implemented in constructed wetlands (CW-MFCs) is low despite the enrichment of anode electricigens most closely related to Geobacter lovleyi. Using the model representative G. lovleyi strain SZ, we show that acetate, but not formate or lactate, can be oxidized efficiently but growth is limited by the high sensitivity of the bacterium to oxygen. Acetate and highly reducing conditions also supported the growth of anode biofilms but only at optimal anode potentials (450 mV vs. standard hydrogen electrode). Still, electrode coverage was poor and current densities, low, consistent with the lack of key c-type cytochromes. The results suggest that the low oxygen tolerance of G. lovleyi and inability to efficiently colonize and form electroactive biofilms on the electrodes while oxidizing the range of electron donors available in constructed wetlands limits MFC performance. The implications of these findings for the optimization of CW-MFCs are discussed (AU)

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Airway epithelium plays a leading role in the complex framework underlying respiratory allergy

Airway epithelium is the cellular structure with the greatest surface exposed to a plethora of environmental airborne substances, including microorganisms, respiratory viruses, air pollutants, and allergens. In addition to being a protective physical barrier at the air-liquid interface, the airway epithelium acts as an effective chemical and immunological barrier that plays a crucial role in orchestrating the immune response in the lungs, by supporting the activation, recruitment, and mobilization of immune cells. Airway epithelium dysfunction has been clearly associated with various airway inflammatory diseases, such as allergic asthma. Although it is not fully understood why a person develops respiratory allergy, a growing body of evidence shows that the nature of the host's immune response is strongly determined by the state of the airway epithelium at the time of contact with the inhaled allergen. Our review highlights the physiological state of airway epithelium as a key element in the development of allergy and, particularly, in exacerbation of asthma. We review the role of physiological oxidants as signaling molecules in lung biology and allergic diseases and examine how high exposure to air pollutants (eg, cigarette smoke and diesel particles) can contribute to the increased incidence of respiratory allergy and exacerbation of the disease (AU)

El epitelio pulmonar constituye la barrera celular más susceptible a la acción deletérea de la multitud de agentes que se encuentran en el ambiente, incluidos los alérgenos. Además de prevenir su acceso al organismo, la barrera epitelial de las vías respiratorias juega un papel inmunomodulador crucial, regulando de forma local la acción de las células del sistema inmune subyacentes. Una disfunción epitelial, provocada tanto directa como indirectamente por la acción de los aeroalérgenos, parece ser una de las causas principales de desregulación de la homeostasis pulmonar, causando una respuesta proinflamatoria descontrolada que cada vez más autores atribuyen al origen de las reacciones alérgicas. En esta revisión se quiere destacar el papel de la barrera epitelial pulmonar como regulador de la respuesta inmune en el contexto de la alergia. Las enfermedades crónicas que afectan a las vías respiratorias, tales como el asma alérgica, muestran frecuentemente una función epitelial defectuosa, apoyando así la hipótesis antes mencionada que subyace al origen de la alergia. El impacto de otros contaminantes ambientales -como virus respiratorios, bacterias, humo del tabaco y partículas diésel- sobre la integridad epitelial, así como su influencia en la biología redox pulmonar relacionada con el desarrollo de la respuesta alérgica, también se abordarán en la presente revisión (AU)

Hypothermia can reverse hepatic oxidative stress damage induced by hypoxia in rats

Our previous findings demonstrated that hypothermia enhances the reduction potential in the liver and helps to maintain the plasmatic antioxidant pool. Here, we aimed to elucidate if hypothermia protects against hypoxia-induced oxidative stress damage in rat liver. Several hepatic markers of oxidative stress were compared in three groups of animals (n = 8 in each group): control normothermic group ventilated with room air and two groups under extreme hypoxia (breathing 10 % O2), one kept at normothermia (HN) (37 °C) and the other under deep hypothermia (HH) (central body temperature of 21-22 °C). Hypoxia in normothermia significantly increased the levels of hepatic nitric oxide, inducible nitric oxide synthase expression, protein oxidation, Carbonilated proteins, advanced oxidation protein products, 4-hydroxynonenal (HNE) protein adducts, and lipid peroxidation when compared to the control group (p < 0.05). However, when hypoxia was induced under hypothermia, results from the oxidative stress biomarker analyses did not differ significantly from those found in the control group. Indeed, 4-HNE protein adduct amounts were significantly lower in the HH versus HN group (p < 0.05). Therefore, hypothermia can mitigate hypoxia-induced oxidative stress damage in rat liver. These effects could help clarify the mechanisms of action of therapeutic hypothermia (AU)

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The new levels of redox regulation of S-adenosylmethionine synthesis / Los nuevos niveles de regulación redox de la síntesis de S-adenosilmetionina

S-adenosylmethionine is a very versatile compound known to be involved in as many reactions as ATP. Its role as methyl donor is key for the production of a large variety of molecules, as well as, for the modification of proteins and nucleic acids. Therefore, it is not surprising that impairments in the methionine cycle are found in many diseases including liver pathologies, Alzheimer or rare diseases. In most of these cases, reductions in S-adenosylmethionine concentrations correlate with the presence of oxidative stress. This fact prompted the study of a putative redox regulation of the methionine cycle that has been focused especially on methionine adenosyltransferases, the enzymes that synthesize S-adenosylmethionine. This review is intended to provide an outline of the new levels at which the redox control of these enzymes is exerted and their importance for liver pathology, a field in which we have made several key contributions

La S-adenosilmetionina es un compuesto muy versátil, conocido por participar en casi tantas reacciones como el ATP. Su papel como donante de grupos metilo es esencial para la producción de una gran variedad de moléculas, así como para la modificación de proteínas y ácidos nucleicos. Por ello, no resulta sorprendente que se hayan detectado alteraciones en el ciclo de la metionina en una gran variedad de patologías, que incluyen desde enfermedades hepáticas hasta el Alzheimer o enfermedades raras. En muchos de estos casos la reducción de los niveles de S-adenosilmetionina se acompaña de la presencia de estrés oxidativo. Este hecho ha inducido el estudio de una posible regulación redox del ciclo de la metionina, que se ha enfocado principalmente a las metionina adenosiltransferasas, que son las enzimas encargadas de la síntesis de S-adenosilmetionina. Esta revisión pretende dar una visión global de los nuevos niveles a los que se ejerce el control redox de estas enzimas y su importancia en hepatopatología, campo en el cual hemos realizado importantes aportaciones

Estudio comparado de la intensidad de entrenamiento sobre la máxima tasa de oxidación de grasas / Effect of training intensity on the fat oxidation rate

Introducción: El ejercicio físico es un importante modulador de la máxima tasa de oxidación de grasas (MFO). Sin embargo, en la relación MFO-ejercicio, las zonas de transición metabólica en la prescripción del ejercicio no son consideradas. Objetivo: Conocer el efecto del entrenamiento en diferentes zonas de transición metabólica sobre la cinética de la MFO y su localización (Fatmax) en jóvenes varones activos. Método: 97 varones fueron distribuidos en 4 grupos homogéneos, 3 experimentales y un grupo control (GC). Cada grupo experimental participó en 8 semanas de entrenamiento administrado de forma continua a intensidad de umbral aeróbico o VT1 (CCVT1), interválica en umbral anaeróbico o VT2 (ITVT2), y en potencia aeróbica máxima o VO2max (ITVO2max). Antes y después del tratamiento los sujetos fueron testados en sendas pruebas con control de gases espirados para determinar el VO2max, VT1 y VT2, y la MFO (calorimetría indirecta) y Fatmax. Resultados: Los resultados muestran un incremento (entre 16,49 y 18,51%; p<0,01) en la MFO en los grupos experimentales. La Fatmax se redujo de media del 60,72±10,52 al 52,35±7,61 %VO2max (p<0,01) por efecto del entrenamiento. El grupo control no experimentó cambios de interés. El análisis intergrupo no presentó diferencias entre los grupos experimentales en ambas variables, sin embargo la comparación contra el GC, reflejó un mayor descenso de la Fatmax en CCVT1 (p<0,05). No se registraron cambios en el rendimiento, salvo un descenso del VO2max en el GC (p<0,05). Conclusión: 8 semanas de entrenamiento de diferente intensidad incrementan la MFO y reducen la Fatmax (AU)

Introduction. Physical exercise is a key modulator of the maximum fat oxidation rate (MFO). However, the metabolic transition zones in the MFO-exercise relationship are not generally considered for training prescription. Objective. To examine the effects of training in different metabolic transition zones on the kinetics of MFO and its localization (Fatmax) in young physically active men. Methods. 97 men were divided into 4 similar sized groups, 3 experimental groups and a control group (CG). Subjects in each experimental group undertook an 8-week running program. Training was continuous at the intensity of the aerobic threshold or VT1 (CCVT1); or performed as intervals at the intensity of the anaerobic threshold or VT2 (ITVT2); or at maximum aerobic power VO2max (ITVO2max). Before and after the training intervention, expired gases were monitored in each subject to determine VO2max, VT1, VT2, MFO (by indirect calorimetry) and Fatmax. Results. In response to training, experimental groups showed an increase in MFO (from 16,49 to 18,51%; p<0,01) and a mean reduction in Fatmax of 60,72±10,52 to 52,35±7,61 %VO2max (p<0,01). No changes of interest were observed in the control subjects. Intergroup comparisons revealed no differences in MFO and Fatmax among the experimental groups, though compared to the CG, a greater reduction in Fatmax was observed in CCVT1 (p<0,05). No changes were detected in performance except a drop in VO2max in the GC (p<0,05). Conclusion. 8 weeks of training led to an increase in MFO and reduction in Fatmax irrespective of training Intensity (AU)

Fluoxetine ameliorates imbalance of redox homeostasis and inflammation in an acute kidney injury model

Ischemia-reperfusion (IR) has been reported to be associated with augmented reactive oxygen radicals and cytokines. Currently, we aimed to examine the influence of fluoxetine, which is already used as a preoperative anxiolytic, in the context of IR induced by occlusion of infrarenal abdominal aorta (60 min of ischemia) and its effects on renal oxidative status, inflammation, renal function, and cellular integrity in reperfusion (120 min post-ischemia). Male rats were randomly assigned as control, IR, and pretreated groups. The pretreated group animals received fluoxetine (20 mg/kg, i.p.) once daily for 3 days. Renal tissue oxidative stress, myeloperoxidase activity, proinflammatory cytokines (tumor necrosis factor-alfa, interleukin-1beta, interleukin-6), histology, and function were assessed. As an anti-inflammatory cytokine, interleukin-10 was also assessed. IR led to a significant increase in lipid hydroperoxide, malondialdehyde, and pro-oxidant antioxidant balance and decrease in superoxide dismutase activity and ferric reducing/antioxidant power level (p < 0.05), but fluoxetine was able to restore these parameters. High concentrations of tumor necrosis factor-alfa, interleukin-1beta, interleukin-6, and myeloperoxidase activity caused by IR were significantly decreased in kidney tissue with fluoxetine. In addition, interleukin-10 levels were high in fluoxetine pretreated group. IR resulted in disrupted cellular integrity, infiltration of tissue with leukocytes, and decreased serum creatinine-urea levels (p < 0.05). Fluoxetine significantly restored impaired redox balance and inflammation parameters of rats subjected to IR to baseline values. This beneficial effect of fluoxetine on redox balance might be addressed to an improvement in renal function (AU)

Marcadores bioquímicos, nutricionales y actividad antioxidante en el síndrome metabólico / Biochemical and nutritional markers and antioxidant activity in metabolic syndrome

ANTECEDENTES Y OBJETIVOS: 1) Valorar nutricionalmente la dieta seguida por los pacientes con síndrome metabólico, y 2) analizar bioquímicamente el nivel de oxidación-reducción en los pacientes con síndrome metabólico. MATERIAL Y MÉTODO: Se trata de un estudio transversal realizado a pacientes con síndrome metabólico de la Región de Murcia. Se seleccionaron 53 individuos, 33 con síndrome metabólico y 20 sin él (grupo control). La intervención realizada consistió en la cumplimentación de una encuesta recordatorio y un test para valorar nutricionalmente la ingesta dietética, además de la determinación de variables antropométricas y analíticas que incluyen variables relacionas con la actividad antioxidante. RESULTADOS: La actividad antioxidante en ambos grupos analizados está dentro de los límites normales (1,7 ± 0,2 mmol/l en el grupo control y 1,8 ± 0,1 mmol/l en el grupo con síndrome metabólico; ns). La enzima superóxido dismutasa no presenta diferencias significativas entre ambos grupos. Los valores medios de glutatión reductasa (U/l) son superiores en el grupo control que en los pacientes con SM (p < 0,05). Respecto a los biomarcadores de estrés oxidativo, los valores medios de isoprostanos son superiores en el grupo control (4,9 ± 6,2 ng/ml) que en los pacientes con SM (3,5 ± 3,9 ng/ml; p < 0,05). Los valores de LDL oxidadas tienden a ser superiores en los enfermos con SM (96 ± 23,2 U/l) que en el grupo control (86,2 ± 17,3 U/l), no observándose diferencias significativas. Conclusiones Existe una tendencia a un peor perfil nutricional y bioquímico de los pacientes que presentan síndrome metabólico. También tienden a presentar un mayor grado de estrés

BACKGROUND AND OBJECTIVES: 1) Nutritional assessment of the diet followed by patients with metabolic syndrome, and 2) biochemical analysis of the oxidation-reduction level in patients with metabolic syndrome. MATERIAL AND METHODS: A cross-sectional study was conducted in patients with metabolic syndrome in Murcia. Fifty-three patients, 33 with and 20 without (control group) metabolic syndrome, were selected. The intervention consisted of completion of a recall survey and a test to nutritionally assess dietary intake. Anthropometric and laboratory variables, including those related to antioxidant activity, were also tested. RESULTS: Antioxidant activity was within normal limits in both groups (1.7 ± 0.2 mmol/L in the control group and 1.8 ± 0.1 mmol/L in the metabolic syndrome group) (NS). Superoxide dismutase levels were not significantly different between the groups. Mean glutathione reductase levels (U/L) were higher in the control group as compared to patients with metabolic syndrome (P < .05). As regards oxidative stress biomarkers, mean isoprostane levels were higher in the control group (4.9 ± 6.2 ng/mL) than in metabolic syndrome patients (3.5 ± 3.9 ng/mL) (P < .05). Oxidized LDL values tended to be higher in metabolic syndrome patients (96 ± 23.2 U/L) as compared to the control group (86.2 ± 17.3 U/L), but differences were not significant. CONCLUSIONS: There is a trend to a poorer nutritional and biochemical profile in patients with metabolic syndrome, who also tend to have a greater degree of oxidative stress

Physical activity and alpha-lipoic acid modulate inflammatory response through changes in thiol redox status

Alpha-Lipoic acid (αLA), as an inductor of hydrogen peroxide (H2O2) and nitrogen oxide (NO) generation and modulator of thiol redox status, plays an important role in cell signalling pathways. The study was designed to observe the effect of AlphaLA on inflammatory response through changes in H2O2 and NO levels as well as thiol redox status. Sixteen physically active males were randomly assigned to one of two groups: placebo or αLA (1,200 mg d(-1) for 10 days prior to exercise). The exercise trial involved a 90-min run at 65% VO2max (0% gradient) followed by 15-min eccentric phase at 65% VO2max (-10% gradient). Blood samples were collected before the exercise trial and then again 20 min, 24, and 48 h after. AlphaLA significantly elevated H2O2 but reduced NO generation before or after exercise. Thiol redox status (GSHtotal-2GSSG/GSSG) increased by > 50% after αLA and exercise (ANOVA, P < 0.05) and correlated with changes in cytokines interleukin-6 (IL-6) (r = -0.478, P < 0.05) and IL-10 (r = -0.455, P < 0.05). This was caused by strong effect of αLA on GSSG concentration. αLA elevated IL-6 and IL-10 levels at 20 min after exercise and decreased in interleukin-1Beta and tumor necrosis factor Alpha before and after exercise. This enhanced the regeneration of injured muscles. Creatine kinase activity tended to lower values after αLA intake. The study suggests that the combination of intense exercise with α-lipoic acid intake might be useful to improve the skeletal muscle regeneration through changes in inflammatory response which are associated with H2O2 and NO generation as well as thiol redox status

Mechanisms associated to impaired activity of cardiac P-type ATPases in endothelial nitric oxide synthase knockout mice

The effect of long-lasting in vivo restriction of nitric oxide (NO) bioavailability on cardiac and renal P-type ATPases critical for intracellular ion homeostasis is controversial. Previous work has shown in eNOS knockout (eNOS−/−) mice hearts that Na+/K+- and Ca2+-ATPase activities were depressed but the underlying mechanisms are still unclear. The goal of this study was to characterize potential alterations responsible for impaired enzyme activity in eNOS−/− mice. Na+/K+-ATPase activity from crude preparations of adult male eNOS−/− mice hearts and kidneys was reduced compared with wild-type animals (32 %, p < 0.05 and 16 %, p < 0.0001, respectively). Immunoblot analysis showed that although the expression of the predominant (or exclusive, for the kidney) Na+/K+-ATPase á1 isoform was not significantly changed, there was an important downregulation of the less abundant á2 isoform in the heart (57 %, p < 0.0001). In addition, although cardiac Ca2+-ATPase activity was unaltered, the expression of sarco/endoplasmic reticulum Ca2+-ATPase 2 protein in eNOS−/− mice was very high (290 % compared with wild-type animals, p < 0.0001) without any significant change in phospholamban expression. Consistent with these findings, the content of cardiac and renal free sulfhydryl groups, essential for the catalytic function of such ATPases, was decreased (23 %, p < 0.01 and 35 %, p < 0.05, respectively). Altogether, the present results suggest that the absence of eNOS promotes a compartmentalized altered redox balance that affects the activity and expression of ion transport ATPases (AU)

Role of the denitrifying Haloarchaea in the treatment of nitrite-brines

Haloferax mediterranei is a denitrifying halophilic archaeon able to reduce nitrate and nitrite under oxic and anoxic conditions. In the presence of oxygen, nitrate and nitrite are used as nitrogen sources for growth. Under oxygen scarcity, this haloarchaeon uses both ions as electron acceptors via a denitrification pathway. In the present work, the maximal nitrite concentration tolerated by this organism was determined by studying the growth of H. mediterranei in minimal medium containing 30, 40 and 50 mM nitrite as sole nitrogen source and under initial oxic conditions at 42 °C. The results showed the ability of H. mediterranei to withstand nitrite concentrations up to 50 mM. At the beginning of the incubation, nitrate was detected in the medium, probably due to the spontaneous oxidation of nitrite under the initial oxic conditions. The complete removal of nitrite and nitrate was accomplished in most of the tested conditions, except in culture medium containing 50 mM nitrite, suggesting that this concentration compromised the denitrification capacity of the cells. Nitrite and nitrate reductases activities were analyzed at different growth stages of H. mediterranei. In all cases, the activities of the respiratory enzymes were higher than their assimilative counterparts; this was especially the case for NirK. The denitrifying and possibly detoxifying role of this enzyme might explain the high nitrite tolerance of H. mediterranei. This archaeon was also able to remove 60 % of the nitrate and 75 % of the nitrite initially present in brine samples collected from a wastewater treatment facility. These results suggest that H. mediterranei, and probably other halophilic denitrifying Archaea, are suitable candidates for the bioremediation of brines with high nitrite and nitrate concentrations (AU)

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Vitamin A supplementation for different periods alters rat vascular redox parameters

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Vitamin A plays physiological and antioxidants properties and is associated with protective effects on arterial level. However, deleterious effects have been reported, including those observed by our group, which has demonstrated pro-oxidant properties in other systems. Therefore, it is needed to better understand the redox effects of retinoids on arterial system. Thus, our aim was to compare vascular redox parameters among animals supplemented or not with vitamin A. Eighty-five adult male rats were treated with different retinyl palmitate (..) (AU)