944 resultados para OXYGEN SPECIES PRODUCTION


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Although the exact cause of neuronal loss in Parkinson's disease is not known, evidence points to oxidative stress and the production of reactive oxygen species as the main events that occur in the substantia nigra pars compacta of the brain of parkinsonians. EGb761 is an extract of the leaves from the Ginkgo biloba tree that has been reported as an antioxidant and neuroprotective agent. The objective of this work was to perform a systematic review of the studies that analysed the effect of Ginkgo biloba extract on Parkinson's disease or Parkinsonism. This research was conducted using the following databases: Medline, PsycInfo, Cinahl, Sigle, Lilacs, Scielo, Cochrane Library, and Embase. Initially, we selected 32 articles. After a more detailed analysis, only 10 articles remained. One of the hypotheses for the positive effect of EGb761 on Parkinson's disease is the reduction or inhibition of monoamine-oxidase activity. This enzyme metabolises dopamine, inducing the formation of free radicals, which in turn damage nigrostriatal neurons. Another hypothesis is that the neuroprotective effect of EGb761 against 6-hydroxydopamine, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and MPP+ toxins. As there are few studies on the effect of EGb761 on humans, this review could contribute new data to further the discussion of this issue.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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The over-production of reactive oxygen species (ROS) can cause oxidative damage to a large number of molecules, including DNA, and has been associated with the pathogenesis of several disorders, such as diabetes mellitus (DM), dyslipidemia and periodontitis (PD). We hypothesise that the presence of these diseases could proportionally increase the DNA damage. The aim of this study was to assess the micronucleus frequency (MNF), as a biomarker for DNA damage, in individuals with type 2 DM, dyslipidemia and PD. One hundred and fifty patients were divided into five groups based upon diabetic, dyslipidemic and periodontal status (Group 1 - poor controlled DM with dyslipidemia and PD; Group 2 - well-controlled DM with dyslipidemia and PD; Group 3 - without DM with dyslipidemia and PD; Group 4 - without DM, without dyslipidemia and with PD; and Group 5 - without DM, dyslipidemia and PD). Blood analyses were carried out for fasting plasma glucose, HbA1c and lipid profile. Periodontal examinations were performed, and venous blood was collected and processed for micronucleus (MN) assay. The frequency of micronuclei was evaluated by cell culture cytokinesis-block MN assay. The general characteristics of each group were described by the mean and standard deviation and the data were submitted to the Mann-Whitney, Kruskal-Wallis, Multiple Logistic Regression and Spearman tests. The Groups 1, 2 and 3 were similarly dyslipidemic presenting increased levels of total cholesterol, low density lipoprotein cholesterol and triglycerides. Periodontal tissue destruction and local inflammation were significantly more severe in diabetics, particularly in Group 1. Frequency of bi-nucleated cells with MN and MNF, as well as nucleoplasmic bridges, were significantly higher for poor controlled diabetics with dyslipidemia and PD in comparison with those systemically healthy, even after adjusting for age, and considering Bonferroni's correction. Elevated frequency of micronuclei was found in patients affected by type 2 diabetes, dyslipidemia and PD. This result suggests that these three pathologies occurring simultaneously promote an additional role to produce DNA impairment. In addition, the micronuclei assay was useful as a biomarker for DNA damage in individuals with chronic degenerative diseases.

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Silicosis, a common type of pneumoconiosis, is an occupational lung disease caused by inhalation of silica dust often with mining activity and thus reaches the miners. The fine and ultrafine silica particles deposited in the alveolar epithelium may lead to the development of progressive massive fibrosis. An increased reactive oxygen species (ROS) production has been proposed to explain the mechanism for induction of pulmonary fibrosis in silicosis. In this situation, alveolar macrophages are activated to phagocytes silica particles deposited in the alveoli. The activated macrophages secrete large amounts of ROS that in turn induce synthesis of fibrotic factors. In addition, the activity of antioxidant enzymes is impaired, which results in increased lipid peroxidation, as well as generating a local inflammatory process. Diffuse pulmonary fibrosis progresses with interstitial collagen deposition. Interstitial collagen overlies small pulmonary arteries and arterioles and thus it is associated with pulmonary hypertension in pulmonary fibrotic diseases. In addition, cytokines and silica particles passing through the respiratory membrane can reach the bloodstream. In this context, the increase in the generation of ROS in the circulation may lead to a reduction in the bioavailability of nitric oxide, an important endothelium-derived relaxing factor. A deficiency in the nitric oxide bioavailability can result in vascular endothelial dysfunction. Moreover, pro-inflammatory cytokines could contribute to the impairment of endothelial function. In the airways, pro-inflammatory cytokines can reduce the smooth muscle responsiveness to β- adrenergic agonists as isoproterenol. Thus, the aim of this study was to evaluate the effect of silica dust instillation in the function of the pulmonary artery, aorta and trachea of rats with acute silicosis. For this purpose, male Wistar rats were anesthetized... (Complete abstract click electronic access below)

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Helicobacter pylori (H. pylori) is a common gastric pathogen that has infected more than 50% of the population of the world and it has been associated with chronic gastritis, gastric ulcers, duodenal ulcer, and gastric cancer. Although, almost all infected people develop gastritis, there is a variety of clinical outcomes, and only a minority (<1%) of infected individuals develop gastric cancer. There are evidences which suggest that the chronic inflammatory reaction caused by the bacterial infection may be involved in the production of reactive oxygen species or reactive nitrogen species. It may lead to DNA damage, which together with the cellular response could lead to gene mutations, chromosomal aberrations characterizing genomic instability that may represent the early step in gastric carcinogenesis. The extent and severity of gastric mucosal inflammation, as well as the clinical outcome of the infection, depend on a number of factors, including the host genetic susceptibility such SNP T3801 CYP1A1, immune response, age at which the infection was acquired, environmental factors, especially dietary and bacterial virulence factors. Due to the risk of developing gastric cancer in humans infected by H. pylori, we used the Comet Assay to investigate the influence of the SNP T3801C CYP1A1 on levels of oxidative DNA damage in gastric epithelial cells. The study was conducted with biopsies from the gastric antrum and corpus of 103 H. pylori-infected patients and 24 uninfected control patients. Genotype of SNP T3801C CYP1A1 was determined by PCR-RFLP and DNA damage levels were measured in gastric mucosal cells from antrum and corpus by the Comet assay. Levels of DNA damage in gastric mucosa cells from antrum and corpus of H. pylori-infected patients with mild, moderate, severe gastritis, and gastric cancer were significantly higher compared to uninfected normal mucosa cells. However, levels... (Complete abstract click electronic access below)