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El rechazo crónico se ha convertido en el mayor desafío a la supervivencia a largo plazo de los trasplantes de órganos sólidos. La generación de especies reactivas del oxígeno es una relevante consecuencia de todos los fenómenos considerados como factores de riesgo de este proceso. Es por esto que resulta de gran interés esclarecer el posible papel patogénico de estas especies químicas en los cambios vasculares que caracterizan la disfunción tardía de los injertos, a la luz de los conocimientos actuales. Se discuten las principales evidencias que permiten establecer un vínculo estrecho entre el daño oxidativo y los mecanismos implicados en la hiperplasia de la íntima, que deterioran funcionalmente los órganos trasplantados a largo plazoThe chronic rejection has become a great challenge to long-term survival of solid organ transplantations. The generation of reactive oxygen species is a relevant consequence of all the phenomena considered as risk factors in this process. This is the reason why the determination of the possible pathogenic role of these chemical species in the vascular changes taking place in late graft failure is of great interest in the light of the present scientific knowledge. The main evidence that make possible to establish a close linking between oxidative damage and the mechanisms involved in intimal hyperplasia that functionally deteriorate transplanted organs in the long run are discussed

La sepsis hoy por hoy continúa siendo un problema de salud, y la morbilidad y mortalidad no han variado a pesar de la introducción de nuevos avances tecnológicos tanto diagnósticos como terapéuticos. En las últimas décadas ha existido una verdadera eclosión en la investigación relativa al papel de los radicales libres y su vinculación con las enfermedades. En el proceso de la sepsis como fenómeno inflamatorio, los órganos y sistemas de órganos que participan no escapan a la acción de los radicales libres; de ahí la necesidad de conocer cómo se involucran los radicales libres en el mecanismo fisiopatológico de estaAt present sepsis is still a health problem and morbidity and mortality have not changed in spite of the introduction of new diagnostic and therapeutic technological advances. During the last decades there has been a real development in the research related to the role of free radicals and their linking with diseases. In the process of sepsis as an inflammatory phenomenon, the organs and systems of organs that take part in it do not escape from the action of free radicals and that's why it is necessary to know how the free radicals involve themselves in its physiopathological mechanism

Introduction: The alpha lipoic acid (ALA) may control and limit the production of free radicals, influencing the development of pathologies such cancer or central sensitization diseases. However, the molecular mechanisms are still not elucidated. Objective: The objective of the present review is to contrast the antioxidant properties of ALA in the prevention and development of pathologies related to the oxidative stress. Materials and methods: In this work, more than 100 articles published during the last 20 years that relate ALA consumption and pathologies related to the oxidative stress have been analysed. The articles have been obtained from different specialized databases (PubMed central, Web of science, Elsevier Journal, Science Direct) and included experiments in animals, cells, and humans. Domains evaluated included ALA, central sensitization diseases, free radicals, and ALA. Results and discussion: Results from in vitro and laboratory animals experiments demonstrate that ALA controls the cell apoptosis of different type of cancers through out the increase of reactive oxygen species, and decrease of cell growth. Moreover, results demonstrated that ALA presents an antioxidant capacity and the ability to regenerate other antioxidants, which is essential to treat the central sensitization diseases. Conclusions: The ALA plays a significant role as antioxidant and prooxidant in cancer and central sensitization diseases, although more extensive studies are required to determine the clinical significance in humans. [ABSTRACT FROM AUTHOR]

Objective: To determine the level of oxidative stress in morbid obese patients by comparing their results to those of a normal population. Material and methods: We have studied the metabolites most representative of OS, both in the blood (MDA, 8-oxo-dG, GSSG and the ratio GSSG/GSH) and in the urine (8-oxo-dG), as well as the GSH antioxidant. A descriptive analysis of the sample was performed. The Kolmogorv-Smirnov test was used to assess whether the distribution of the different metabolites was normal. In the case of normal distribution, the Student's t test was used to compare the means, the Mann-Whitney U test was used for non-parametric data, with a significance level of p < 0.05 for hypothesis contrast. Results: There were 28 patients in each group, without statistically significant differences regarding age and gender. The group of patients with morbid obesity presented an average BMI of 50.1 ± 4 and 23.9 ± 6 in the group with normal weight. 67.8% of the patients with morbid obesity had other comorbidities. There were no associated pathologies in the control group. All the values for the different OS metabolites were higher in the group of patients with morbid obesity than in the control group, whereas the activity of the antioxidant systems (GSH) was lower in the group with morbid obesity. Conclusion: The figures of OS metabolites obtained in the group of patients with morbid obesity confirm the presence of OS in obesity at a pathological level given the differences obtained in the group of normal population. [ABSTRACT FROM AUTHOR]

Ulomoides dermestoides is a tenebrionidae beetle, used in China as an aphrodisiac and nutracetical food. In Colombia, these beetles are eaten alive in the treatment of some illnesses such as bronchial asthma and rheumatoid arthritis. The aims of this research were determinated the total phenolic content and free radical scavenging activity of hidromethanolic extracts of Ulomoides dermestoides adults. The extracts were obtained with MeOH 48% and the phenolic compounds were separated by column chromatography on Amberlite XAD- 2 resin. The total phenolic content was determinated by using the Folin-Ciocalteu assay and the results were expressed as milligrams of gallic acid equivalent per gram of dry weight (GAE mg/g ES). The radical scavenging activity was measured according to DPPH• and ABTS•+ methods and the results were expressed as the percentage of radical scavenging (% CR). The total phenolic content in the Ulomoides dermestoides extract was 22.94 ± 0.34 mg GAE /gES, % CR by DPPH• and ABTS•+ were 90.62 ± 1.1 and 98.11 ± 0.84, respectively. All phenolic fractions showed free radical scavenging activity, however fractions separated with MeOH had a higher activity. These results indicate that Ulomoides dermestoides beetle is source of antioxidants and this compounds could be used as nutraceuticals. [ABSTRACT FROM AUTHOR]

Copyright of Revista Médica de Risaralda is the property of Universidad Tecnologica de Pereira and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Antioxidants are substances that may protect cells against the effects of free radicals. Low levels of antioxidants, or inhibition of the antioxidant enzymes, cause oxidative stress and may damage occurs causing oxidize of the proteins, lipids and Deoxyribonucleic Acid. Previous studies correlate the relationship between oxidative stress and the pathogenesis of numerous diseases such as Parkinson's disease, cancer and infertility. The use of antioxidant supplements to prevent some diseases has been studied. Antioxidants play an important role in prevention of chronic diseases. The consumption of such compounds can be formed either by enzymatic, non enzymatic or the innovation of chemical compounds with enzymatic antioxidant activity supporting the positive effects on patient health. [ABSTRACT FROM AUTHOR]

Copyright of Revista Veterinaria is the property of Universidad Nacional del Nordeste and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

After traumatic spinal cord injury (TSCI) decrease glycine level. The effects of administration of glycine are not fully understood. Objective: evaluate functional motor recovery of TSCI in rats after administration of glycine. Material and method: TSCI was made in T8, under anesthesia in two groups Wistar rats. One group received glycine (TSCI+GLI), the other (TSCI+VEH) and healthy rats group received vehicle. After the lesion, the spasticity and motor performance was assessed after TSCI using beam-walking paradigm and the footprint analysis for 8 weeks. Results: after the lesion, spasticity and beam-walking and footprint analysis showed an important motor deficit. Moreover, a slightly improvement were observed in the TSCI+GLI group, although no significant differences were found when the TSCI+GLI and TSCI+VEH groups were compared. Conclusions: the motor alteration taken place by the TSCI was valued appropriately by the battery of tests used motor performance. The glycine didn't produce an effect statistically significant on the recovery of the complex patterns of sensory-motor integration after the TSCI, suggesting the use of different glycine dose and of pharmaceutical that inhibit the formation of free radicals, inflammatory reaction, such cyclosporin-A, and deferoxamine to completely abolish the oxidative effect of ferrous iron. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is a chronic-degenerative disease with a high incidence and prevalence around the world. Chronic hyperglycemia, a feature of diabetes, induces a higher production of superoxide free radicals, which play a major role in the mechanisms of tissue damage responsible for the clinical complications of DM: advanced glycosylation and activation of sorbitol, hexosamines, and protein kinase C pathways. Although diferent drugs that inhibit the damaging pathways have been developed, their actual benefit in diabetic patients has not been proved yet. Therefore, adequate glycemia control is still the fundamental factor to prevent or delay tissue damage. [ABSTRACT FROM AUTHOR]

Copyright of Cirugía y Cirujanos is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cogitare Enfermagem is the property of Cogitare Enfermagem and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista de la Sociedad Química del Perú is the property of Sociedad Quimica del Peru and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The denominated biological dosimetry by espectroscopy of electronic paramagnetic resonance (EPR) in irradiated sanguineous fluids requires of an special process of the sample, with the purpose of obtaining good results and of developing a correct analysis. For it they are due to consider like fundamental parameters of analysis: the factor of Landé (g) of the sample, the type and volume of sample, the type of ionizing radiation, the temperature of analysis, the time of analysis, the concentration of spins (concentration of free radicals) and the time of relaxation spin-spin. In this work you can see a simple protocol of the results of samples of human blood. The samples radiated with gammas of Co60 of a Theratron 780 between plaques of PMMA to a depth of Zmáx = 0.5cm and with electrons of energy of 6MeV between plaques of PMMA to a depth of Zmáx = 1.5cm in ranges of doses from 5 to 15Gy. [ABSTRACT FROM AUTHOR]

Introduction: Physical activity conduces to oxidative stress, which produces undesirable effects. However, it is well known that free radicals, when present in low concentrations, also have physiological effects in the exercise adaptation process. In addition, the majority of antioxidant supplementation studies, in spite of the fact of decreases oxidative stress, have failed to show a performance improving. Objectives: The goals of this review are to reinterpret the available evidence about the role of free radicals in exercise, and to analyze why antioxidant supplementation have not shown the expectable ergogenic effect. Methods: The following topics were reviewed: i) the free radical biology; ii) antioxidant systems; iii) exercise induced-oxidative stress; iv) oxidative stress and physical performance; and v) antioxidant supplementation and physical performance. Results: There is evidence that physical exercise is associated with excessive free radical production. Deleterious effects of free radicals in physical performance have been shown by in situ studies, although evidence in humans is also available. Physical exercise results in muscular hypoxia, which conduces to adaptative responses, probably through free radical-mediated HIF-1α stabilization. Moreover, a certain level of free radicals is necessary for optimal muscle contractility. Conclusions: Free radicals are necessary for exercise-induced hypoxia adaptation and muscle contraction, for that reason long term antioxidant supplementation interfere with its physiological role. This, explain why antioxidants decrease oxidative stress markers but fail to improve physical performance. [ABSTRACT FROM AUTHOR]

At the present time the ingestion of foods and drinks manufactured with sweeteners has been increased, and aspartame (Asp) is the most used sweetener in food elaboration for children and adults, in more than 90 countries. Recent studies have related the consumption of Asp to the development of metabolic alterations and the increase of neurological disorders associated with the production of free radicals and lipid peroxidation products. The aim of this study was to evaluate the effect of the Asp in the brain of rats by means of the determination of the levels of Glutathion (GSH) and the concentration of thiobarbituric acid reactive substances through the lipid peroxidation (TBARS). Material and methods: male Wistar rats of 21 days old were administered with Asp 75mg/kg and 125mg/kg, phenylalanine 62.5mg/kg, Aspartic acid 50mg/kg, all by oral route, for 30 consecutive days. At the end of the study the animals were sacrificed and the brain was homogenated for GSH and TBARS levels determination. Results: The GSH levels were significantly decreased (p<0.05), in all the groups that received Asp, phenylalanine and aspartic acid, with respect to the control group. The TBARS concentration was significantly increased only in the animals with treatment with Asp in 125mg/kg dose versus group control. Conclusion: the results suggest that the administration of high doses of Asp unprotect the brain, exposing it to oxidative damage. [ABSTRACT FROM AUTHOR]

Copyright of Universitas Médica is the property of Pontificia Universidad Javeriana and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The article examines the antioxidant activity potential of Bauhinia Kalbreyeri Harms. The authors explain that the plant has been determined by the Colombian ethnomedicine as antidiabetic. They evaluate the extracts for free radicals by DPPH method. Ethanol mixed on the extracts showed the higher DPPH radical scavenging activity than 90% in almost all the concentration tested.

The evolution and development of currently know organisms, comprised their change and adaptation from the reducing atmosphere to an oxidizing one. The adaptive changes show that some processes were developed to take advantage of the oxidizing atmosphere efficiently. The most important adaptive change was the efficiency in the energy production of aerobic organisms. Some toxic wastes of this process, known as reactive oxygen species, have deleterious functions when modifying and damaging structural and metabolic components of the cells. For this reason, in a parallel way, the processes of evolutionary adaptation included the formation of antioxidant compounds to protect cells from oxidative damage. Nevertheless, under certain circumstances these reactive oxygen species can have paradoxical functions such as the induction of proliferation and cellular death, which occurs in cancer and apoptosis. [ABSTRACT FROM AUTHOR]

A person who practices exercise in a routinely way increases the production of reactive oxygen species in his tissues, mainly as a result of oxygen's oxidation in the mitochondria. An important damage to the tissues and the cell are produced by reactive oxygen species, so it has been suggested that ingestion of antioxidant supplements (mainly vitamin A, C and E) can diminish this damage. It has also spread the idea that ingestion of antioxidant supplements can improve the physical yield of an athlete, but there is no evidence to support such asseveration. This article is a briefly review of the possible protective effects of antioxidant supplements against the reactive oxygen species produced in people who practices exercise. [ABSTRACT FROM AUTHOR]

Oxidative stress plays a crucial role in the pathology of neurodegenerative diseases such as Alzheimer's Parkinson's, Huntington and amyotrophic lateral sclerosis as well. Increased markers of oxidative damage are present in such conditions. They involve protein, lipids, DNA and even RNA oxidation. Several evidences indicate that increase in reactive oxygen species, an antioxidant systems deficit, decreased repair DNA mechanisms, proteolysis and the loss of immune system regulation are contributing factors to an increased oxidative stress. All those processes ultimately lead to a progressive neuronal death and damage. Alzheimer's a neurofibrillary tangles disorder, Parkinson's disease, a decrease in dopaminergic neurons, Huntington's, a loss of neostriatal neurons and Amyotrophic lateral sclerosis, a motor neuron disease, are common neurodegenerative diseases. Although these disorders differ from important pathways, they share some pathogenic features including inflammation, genetic mutations and inappropriate protein aggregates (Lewy bodies, amyloid plaques). Glial activation and dysfunction in dopaminergic, cholinergic and gabaergic systems are also common. Oxidative stress and mitochondrial dysfunction that eventually lead to neuronal death play a fundamental in the progressive impairment that patients with that kind of neurodegenerative diseases show. In current review, aspects that closely associate an oxidative stress state to neurodegeneration processes occurring in some neuropathologic conditions. [ABSTRACT FROM AUTHOR]

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Electron paramagnetic resonance (EPR) spectra in samples of demineralized water, blood, and sanguineous plasma were obtained. For demineralized water, the spectra were analyzed before radiating and after irradiation, with a dosage of 5 Gy. The results show the presence of signals with values of g ≈ 2.13 and 2.41 in plasma, blood, and radiated water. For the first g values, some authors have associated such to free radicals like: globin (Fe(IV)=0) or Cu2+ incorporated to the ceruplasmin molecule. [ABSTRACT FROM AUTHOR]

Free radicals constitute an important threat to the organism, in defense, cells have developed several antiuxidant enzymes, superoxide dismutase (SOD), catalase and glutathione peroxidase. SOD is in charge of the removal of superoxide radicals produced in the mitochondrial electron transport chain. Objective: To determine and compare SOD levels of a high altitude and sea level population. Materials and Methods: This was a descriptive study. Blood samples were taken from blood donors of blood banks of Hospital Nacional Cayetano Heredia in Lima and Hospital Victor Ramos Guardia in Huaraz (3 052 meters above sea level). Ninety seven samples were analyzed using the Minami and Yoshikawa method to determine SOD activity. Results: The means for SOD values were 1 834 U/gr.Hb for Lima and 926.5 U/gr.Hb for Huaraz (p < 0.05). In every age group the high altitude natives had lower levels of SOD than the ones at sea level. There was a significant difference between women from Lima and Huaraz (1 929 U/gr.Hb vs. 941.89 U/gr.Hb; p < 0.05). The same was observed when comparing means of men from Lima and Huaraz (1 754 U/gr.Hb vs. 907.78 U/ gr.Hb; p < 0.05). Conclusions: High altitude natives have lower levels of SOD. [ABSTRACT FROM AUTHOR]

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Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objectives: To demonstrate that nitric oxide (NO) contributes to free radical generation after epicardial shocks and to determine the effect of a nitric oxide synthase (NOS) inhibitor, NG-nitro-l-arginine (l-NNA), on free radical generation. Background: Free radicals are generated by direct current shocks for defibrillation. NO reacts with the superoxide (O2⋅−) radical to form peroxynitrite (O=NOO−), which is toxic and initiates additional free radical generation. The contribution of NO to free radical generation after defibrillation is not fully defined. Methods and results: Fourteen open chest dogs were studied. In the initial eight dogs, 40 J damped sinusoidal monophasic epicardial shocks was administered. Using electron paramagnetic resonance, we monitored the coronary sinus concentration of ascorbate free radical (Asc⋅−), a measure of free radical generation (total oxidative flux). Epicardial shocks were repeated after l-NNA, 5 mg/kg IV. In six additional dogs, immunohistochemical staining was done to identify nitrotyrosine, a marker of reactive nitrogen species-mediated injury, in post-shock myocardial tissue. Three of these dogs received l-NNA pre-shock. After the initial 40 J shock, Asc⋅− rose 39±2.5% from baseline. After l-NNA infusion, a similar 40 J shock caused Asc⋅− to increase only 2±3% from baseline (P<0.05, post-l-NNA shock versus initial shock). Nitrotyrosine staining was more prominent in control animals than dogs receiving l-NNA, suggesting prevention of O=NOO− formation. Conclusions: NO contributes to free radical generation and nitrosative injury after epicardial shocks; NOS inhibitors decrease radical generation by inhibiting the production of O=NOO−. [Copyright &y& Elsevier]

Background: During reperfusion of ischemic myocardium nitric oxide (NO) reacts with superoxide radicals to form cardiotoxic peroxynitrite, which causes lipid peroxidation. Our hypothesis was that infusion of a NO donor S-nitroso-N-acetylpenicillamine (SNAP) during ischemia–reperfusion would exacerbate the oxidative damage to the myocardium by increased formation of nitrogen radicals. Methods and results: In 19 open-chest dogs, left anterior descending (LAD) coronary occlusion (15 min)–reperfusion (15 min) sequences were created. Using electron paramagnetic resonance (EPR), we monitored the coronary sinus concentration of ascorbate free radical (Asc⋅−), a measure of free radical generation (total oxidative flux). Seven control dogs (Group 1) received intravenous saline infusion during occlusion–reperfusion, while 12 dogs received SNAP infusion (Group 2: 2.5 μg/min per kg SNAP, and Group 3: 5 μg/min per kg SNAP). Left ventricular fractional area shortening was determined by echocardiography. Dogs in Group 3 receiving a high dose of SNAP (5 μg/min per kg) demonstrated a higher Asc⋅− concentration increase than the control group. Percent fractional area shortening in Group 1 declined from 77±4.0 (baseline) to 54±9.0% during ischemia (P<0.05), and then fully recovered to 74±3.7% with reperfusion. In the SNAP-treated dogs, the percent fractional area shortening during reperfusion was significantly lower than baseline in Group 2 (55±3.9 vs. baseline 74±4.4%, P<0.05) and in Group 3 (49±5.0 vs. baseline 71±4.5%, P<0.01). In five additional dogs, nitrotyrosine immunohistochemistry showed heavy staining of the ischemic-reperfused myocardium. Conclusions: The NO donor SNAP increased free radical concentration and exacerbated myocardial oxidative damage after ischemia–reperfusion. [Copyright &y& Elsevier]

Objectives: To demonstrate that nitric oxide (NO) contributes to free radical generation after epicardial shocks and to determine the effect of a nitric oxide synthase (NOS) inhibitor, NG-nitro-l-arginine (l-NNA), on free radical generation. Background: Free radicals are generated by direct current shocks for defibrillation. NO reacts with the superoxide (O2⋅−) radical to form peroxynitrite (O&z.dbnd6;NOO−), which is toxic and initiates additional free radical generation. The contribution of NO to free radical generation after defibrillation is not fully defined. Methods and results: Fourteen open chest dogs were studied. In the initial eight dogs, 40 J damped sinusoidal monophasic epicardial shocks was administered. Using electron paramagnetic resonance, we monitored the coronary sinus concentration of ascorbate free radical (Asc⋅−), a measure of free radical generation (total oxidative flux). Epicardial shocks were repeated after l-NNA, 5 mg/kg IV. In six additional dogs, immunohistochemical staining was done to identify nitrotyrosine, a marker of reactive nitrogen species-mediated injury, in post-shock myocardial tissue. Three of these dogs received l-NNA pre-shock. After the initial 40 J shock, Asc⋅− rose 39±2.5% from baseline. After l-NNA infusion, a similar 40 J shock caused Asc⋅− to increase only 2±3% from baseline (P<0.05, post-l-NNA shock versus initial shock). Nitrotyrosine staining was more prominent in control animals than dogs receiving l-NNA, suggesting prevention of O&z.dbnd6;NOO− formation. Conclusions: NO contributes to free radical generation and nitrosative injury after epicardial shocks; NOS inhibitors decrease radical generation by inhibiting the production of O&z.dbnd6;NOO−. [Copyright &y& Elsevier]

Objective: Our objective was to determine if magnesium reduces free radicals generated by direct current countershock and preserves left ventricular contractile function. Background: We have previously shown that magnesium reduces free radicals in a coronary occlusion-reperfusion model, and therefore also might reduce free radical generation by direct current shocks. Methods: In eight swine weighing 18–27 kg (mean: 22 kg), using electron paramagnetic resonance, we monitored continuously the coronary sinus concentration of ascorbate free radical, a measure of free radical generation (total oxidative flux). Epicardial shocks (30 J) using a truncated exponential biphasic waveform (5/5 ms) were administered. Each animal received two shocks, one without and one with magnesium, 80 mg/min IV, beginning 10 min before the shock and continuing to 15 min after the shock. Percent fractional area shortening of the left ventricular cavity was determined by 2-dimensional echocardiography. Results: Magnesium shocks resulted in a significantly lower increase in the ascorbate free radical concentration (0.6±4.6%) than no-magnesium shocks (16±3.3%, P<0.05) at 12 min after the shock. Total radical flux was reduced 72% (P<0.05), and left ventricular fractional area shortening was preserved: baseline: 69±2.6%, no-magnesium shocks: 41±2.8% (P<0.05, versus baseline) and magnesium shocks 61±3.7%. Conclusions: Magnesium pre-treatment reduced oxygen free radicals generated by direct current shocks; post-shock left ventricular contractile function was not impaired. Magnesium may be cardioprotective during epicardial (‘surgical’) defibrillation. [Copyright &y& Elsevier]

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Copyright of Journal of Physiology & Biochemistry is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

El artículo examina el rol del óxido nítrico como mediador de disfunción endotelial. Se menciona que los estados inflamatorios recurrentes de infección son unas de las consecuencias debidos a disfunción endotelial. El óxido nítrico no es sólo un mediador de la fisiología vascular, sino también actúa como una sustancia metabólicamente activa. El artículo habla de su papel con otros mediadores como las moléculas de adhesión y los radicales libres.

Los embriones producidos in vitro (EPIV) presentan bloqueo en eldesarrollo en el momento de la activación del genoma (8-16 células en bovinos), limitando la producción de blastocitos (35%). Este fenómeno ha sido relacionado con la producción de Especies Reactivas de Oxígeno (ERO). Entre las fuentes de ERO se han descrito altas tensiones de oxígeno, exposición a la luz y alteración del metabolismo oxidativo (1). Los EPIV con baja competencia para superar el bloqueo presentan fallas en la funcionalidad mitocondrial (1) y nucleolar, exhibiendo un retardo en su tasa de clivaje (2). Algunos autores han relacionado el tiempo al primer clivaje con la cantidad relativa de ciertostranscriptos, como Glutatión (2), un limpiador de ERO, sugiriendo que los embriones incompetentes presentan fallas transcripcionales que les impiden defenderse contra las ERO producidas en cultivo, quizás manteniendo niveles elevados de H2O2 lo que los hace más susceptibles al daño celular.Hasta el presente no se ha efectuado un estudio de cinética de producción de ERO, en EPIV bovinos con alta y baja competencia durante el desarrollo temprano, ni se ha logrado esclarecer el papel de la mitocondria en la generación de ERO (como fuente o como blanco).Los objetivos de este estudio son determinar la cinética de producción de H2O2 en embriones con alta y baja competencia para superar el bloqueo y la relación de éstos con procesos de daño mitocondrial y mortalidad embrionaria.

El estrés oxidativo se define como el desequilibrio entre la generaciónde especies reactivas del oxígeno (ERO) y la cantidad de enzimasy compuestos antioxidantes. En malaria las ERO son producidas por el hospedero con el objetivo de controlar la parasitemia y por el parásito directamente al degradar la hemoglobina. En este trabajo se evaluó el estrés oxidativo de pacientes infectados con P. falciparum o P. vivax, cuantificando los niveles de malondialdehído (MDA), el estado de antioxidantes totales y la actividad de las enzimas catalasa, superóxidodismutasa y glutatión- peroxidasa intraeritrocitarias.

Copyright of West Indian Medical Journal is the property of West Indian Medical Journal (WIMJ) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)