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1.
Oxid Med Cell Longev ; 2021: 3790477, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34790285

RESUMO

Low-ozone doses cause alterations in the oxidation-reduction mechanisms due to the increase in reactive oxygen species, alter cell signaling, and produce deleterious metabolic responses for cells. Adenosine 5'triphosphate (ATP) can act as a mediator in intercellular communication between neurons and glial cells. When there is an increase in extracellular ATP, a modification is promoted in the regulation of inflammation, energy metabolism, by affecting the intracellular signaling pathways that participate in these processes. The objective of this work was to study changes in the P2X7 receptor, and their relationship with the inflammatory response and energy metabolism, in a model of progressive neurodegeneration in the hippocampus of rats chronically exposed to low-ozone doses. Therefore, 72 male rats were exposed to low-ozone doses for different periods of time. After exposure to ozone was finished, rats were processed for immunohistochemical techniques, western blot, quantitative polymerase chain reaction (qPCR), and histological techniques for periodic acid-Schiff staining. The results showed immunoreactivity changes in the amount of the P2X7 protein. There was an increase in phosphorylation for glycogen synthase kinase 3-ß (GSK3-ß) as treatment continued. There were also increases in 27 interleukin 1 beta (IL-1 ß) and interleukin 17 (IL-17) and a decrease in interleukin 10 (IL-10). Furthermore, neuronal glycogen was found at 30 and 60 days, and an increase in caspase 3. An increase in mRNA was also shown for the P2X7 gene at 60 days, and GSK3-ß at 90 days of exposure. In conclusion, these results suggest that repeated exposure to low-ozone doses, such as those that can occur during highly polluted days, causes a state of oxidative stress, leading to alterations in the P2X7 receptors, which promote changes in the activation of signaling pathways for inflammatory processes and cell death, converging at a progressive neurodegeneration process, as may be happening in Alzheimer's disease.


Assuntos
Hipocampo/patologia , Doenças Neurodegenerativas/patologia , Doenças Neuroinflamatórias/patologia , Neurônios/patologia , Ozônio/toxicidade , Receptores Purinérgicos P2X7/metabolismo , Trifosfato de Adenosina/metabolismo , Animais , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Interleucina-1beta/metabolismo , Masculino , Doenças Neurodegenerativas/induzido quimicamente , Doenças Neurodegenerativas/metabolismo , Doenças Neuroinflamatórias/induzido quimicamente , Doenças Neuroinflamatórias/metabolismo , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Oxidantes Fotoquímicos/toxicidade , Estresse Oxidativo , Ratos , Ratos Wistar , Receptores Purinérgicos P2X7/genética
2.
Neuroscience ; 252: 384-95, 2013 Nov 12.
Artigo em Inglês | MEDLINE | ID: mdl-23988432

RESUMO

The aim of this study was to analyze the effects of chronic oxidative stress on mitochondrial function and its relationship to progressive neurodegeneration in the hippocampus of rats chronically exposed to ozone. Animals were exposed to 0.25 ppm ozone for 7, 15, 30, or 60 days. Each group was tested for (1) protein oxidation and, manganese superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx) and succinate dehydrogenase (SDH) activity using spectrophotometric techniques, (2) oxygen consumption, (3) cytochrome c, inducible nitric oxide synthase (iNOS), peroxisome proliferator-activated receptor γ Co-activator 1α (PGC-1α), B-cell lymphoma (Bcl-2), and Bax expression using Western blotting, (4) histology using hematoxylin and eosin staining, and (5) mitochondrial structure using electron microscopy. Our results showed increased levels of carbonyl protein and Mn-SOD activity after 30 days of ozone exposure and decreased GPx activity. The SDH activity decreased from 7 to 60 days of exposure. The oxygen consumption decreased at 60 days. Western blotting showed an increase in cytochrome c at 60 days of ozone exposure and an increase in iNOS up to 60 days of ozone exposure. The expression of PGC-1α was decreased after 15, 30, and 60 days compared to the earlier time Bcl-2 was increased at 60 days compared to earlier time points, and Bax was increased after 30 and 60 days of exposure compared to earlier time points. We observed cellular damage, and mitochondrial swelling with a loss of mitochondrial cristae after 60 days of exposure. These changes suggest that low doses of ozone caused mitochondrial abnormalities that may lead to cell damage.


Assuntos
Hipocampo/metabolismo , Hipocampo/patologia , Mitocôndrias/metabolismo , Mitocôndrias/patologia , Estresse Oxidativo/fisiologia , Animais , Western Blotting , Imuno-Histoquímica , Oxidantes Fotoquímicos/toxicidade , Ozônio/toxicidade , Ratos , Ratos Wistar
3.
Rev Neurosci ; 24(3): 337-52, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23585211

RESUMO

Ozone (O3) is a component of photochemical smog, which is a major air pollutant and demonstrates properties that are harmful to health because of the toxic properties that are inherent to its powerful oxidizing capabilities. Environmental O3 exposure is associated with many symptoms related to respiratory disorders, which include loss of lung function, exacerbation of asthma, airway damage, and lung inflammation. The effects of O3 are not restricted to the respiratory system or function - adverse effects within the central nervous system (CNS) such as decreased cognitive response, decrease in motor activity, headaches, disturbances in the sleep-wake cycle, neuronal dysfunctions, cell degeneration, and neurochemical alterations have also been described; furthermore, it has also been proposed that O3 could have epigenetic effects. O3 exposure induces the reactive chemical species in the lungs, but the short half-life of these chemical species has led some authors to attribute the injurious mechanisms observed within the lungs to inflammatory processes. However, the damage to the CNS induced by O3 exposure is not well understood. In this review, the basic mechanisms of inflammation and activation of the immune system by O3 exposure are described and the potential mechanisms of damage, which include neuroinflammation and oxidative stress, and the signs and symptoms of disturbances within the CNS caused by environmental O3 exposure are discussed.


Assuntos
Sistema Nervoso/efeitos dos fármacos , Oxidantes Fotoquímicos/toxicidade , Ozônio/toxicidade , Poluentes Atmosféricos/toxicidade , Animais , Exposição Ambiental , Humanos , Sistema Nervoso/metabolismo , Pneumonia/induzido quimicamente , Pneumonia/metabolismo
4.
Toxicol Mech Methods ; 20(1): 25-30, 2010 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-20017603

RESUMO

Ozone is a molecule of high energetic content. Its great oxidative power has been used in medicine for the treatment of several illnesses with a wide spectrum. The rectal insufflation with a mixture of ozone/oxygen is considered as a simple therapy, not painful, of low cost and practically free from adverse effects. Given its potential oxidation and lack of side-effects, the objective has been to know the state of different indexes of redox state in blood which may contribute to understanding the mechanism by which mixtures of ozone/oxygen administered by intrarectal route are able to exert actions on other organs. With this purpose female rabbits were used, distributed into four groups, and three doses of ozone/oxygen mixture were tested. When treatment was finished, the determination of pro-oxidant and antioxidant markers was carried out. Also indexes of organic damage were determined. Ozone doses administered to rabbits did not cause adverse effects and mortality did not show significant changes relative to tissue damages and they increased enzymes activities belonging to the first line antioxidant defences. The results demonstrate that ozone/oxygen mixture administered by rectal insufflations is innocuous and it is able to increase the antioxidant defense of the organism.


Assuntos
Oxidantes Fotoquímicos/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Oxigênio/toxicidade , Ozônio/toxicidade , Administração Retal , Animais , Biomarcadores/metabolismo , Feminino , Longevidade/efeitos dos fármacos , Estresse Oxidativo/fisiologia , Coelhos , Testes de Toxicidade
5.
Cad Saude Publica ; 25(8): 1791-6, 2009 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-19649420

RESUMO

The aim of this study was to assess the association between prenatal exposure to air pollutants and low birth weight in a medium-sized city. An ecological study was performed, using live birth data from São José dos Campos, São Paulo State, Brazil. The environmental data were obtained from the São Paul State Environmental Agency. The study included full-term newborns whose mothers were 20 to 34 years of age and had at least a complete high school education, seven or more prenatal visits, singleton pregnancy, and vaginal delivery, in order to minimize potential confounding from these variables. Logistic regression was used to estimate the effect of each pollutant. Low birth weight was defined as less than 2,500 g. The sample included a total of 2,529 data from 2001 that met the inclusion criteria (25.6% of the total). We identified 99 newborns (3.95% of the sample) with low birth weight, and the pollutants sulfur dioxide and ozone were associated with low birth weight. The final model was A(x) = -1.79 + 1.30 (SO2) + 1.26 (O3). Thus, sulfur dioxide and ozone were identified as risk factors for low birth weight in a medium-sized city in Southeast Brazil.


Assuntos
Poluentes Atmosféricos/toxicidade , Peso ao Nascer/efeitos dos fármacos , Recém-Nascido de Baixo Peso , Exposição Materna/efeitos adversos , Ozônio/toxicidade , Dióxido de Enxofre/toxicidade , Adulto , Brasil/epidemiologia , Feminino , Humanos , Recém-Nascido , Modelos Logísticos , Exposição Materna/estatística & dados numéricos , Razão de Chances , Oxidantes Fotoquímicos/toxicidade , Material Particulado/toxicidade , Gravidez , Cuidado Pré-Natal , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Fatores de Risco , População Urbana
6.
Cad. saúde pública ; 25(8): 1791-1796, ago. 2009. tab
Artigo em Inglês | LILACS | ID: lil-520751

RESUMO

The aim of this study was to assess the association between prenatal exposure to air pollutants and low birth weight in a medium-sized city. An ecological study was performed, using live birth data from São José dos Campos, São Paulo State, Brazil. The environmental data were obtained from the São Paul State Environmental Agency. The study included full-term newborns whose mothers were 20 to 34 years of age and had at least a complete high school education, seven or more prenatal visits, singleton pregnancy, and vaginal delivery, in order to minimize potential confounding from these variables. Logistic regression was used to estimate the effect of each pollutant. Low birth weight was defined as less than 2,500g. The sample included a total of 2,529 data from 2001 that met the inclusion criteria (25.6 percent of the total). We identified 99 newborns (3.95 percent of the sample) with low birth weight, and the pollutants sulfur dioxide and ozone were associated with low birth weight. The final model was À(x) = -1.79 + 1.30 (SO2) + 1.26 (O3). Thus, sulfur dioxide and ozone were identified as risk factors for low birth weight in a medium-sized city in Southeast Brazil.


O objetivo foi estimar o papel de poluentes no baixo peso ao nascer numa cidade de porte médio. Foi um estudo ecológico com dados obtidos da Declaração de Nascido Vivo relativos a São José dos Campos, São Paulo, Brasil. Os dados ambientais foram fornecidos pela Companhia de Tecnologia de Saneamento Ambiental (CETESB). Foram incluídos no estudo recém-nascidos a termo, com mães entre 20 e 34 anos de idade, segundo grau completo, sete ou mais consultas realizadas no pré-natal, gravidez única e parto normal, para minimizar o efeito de confusão destas variáveis. Utilizou-se regressão logística para estimar o efeito de cada poluente. Baixo peso ao nascer foi considerado aquele inferior a 2.500g. Foram incluídos 2.529 dados de 2001 que atenderam aos critérios de inclusão (25,6 por cento do total). Identificamos 99 recém-nascidos (3,95 por cento dessa amostra) com baixo peso e os poluentes dióxido de enxofre e ozônio como associados ao baixo peso ao nascer. O modelo final foi À(x) = -1,79 + 1,30 (SO2) + 1,26 (O3). Assim, identificou-se o dióxido de enxofre e ozônio como responsáveis pelo baixo peso ao nascer numa cidade de porte médio do Sudeste brasileiro.


Assuntos
Adulto , Feminino , Humanos , Recém-Nascido , Gravidez , Poluentes Atmosféricos/toxicidade , Peso ao Nascer/efeitos dos fármacos , Recém-Nascido de Baixo Peso , Exposição Materna/efeitos adversos , Ozônio/toxicidade , Dióxido de Enxofre/toxicidade , Brasil/epidemiologia , Modelos Logísticos , Exposição Materna/estatística & dados numéricos , Razão de Chances , Oxidantes Fotoquímicos/toxicidade , Cuidado Pré-Natal , Material Particulado/toxicidade , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Fatores de Risco , População Urbana
7.
Mutat Res ; 675(1-2): 41-5, 2009 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-19386246

RESUMO

The aims of this study were to investigate the sensitivity of Tradescantia pallida 'Purpurea' to genotoxicity induced by ozone, by means of the micronucleus (MCN) bioassay, to verify whether the intensity of genotoxic responses in inflorescences is modulated by concentrations of ascorbic acid (AA) in their bracts, and/or by air temperature variations during the progress of the bioassay, and to define the time lag necessary after ozone exposure to observe maximal genotoxic effects. Flowering branches were exposed to filtered air (control) and to 60 ppb of ozone (ozone) for 3h in fumigation chambers during spring, autumn, winter and summer. After exposure, they were maintained for 24-120 h under filtered air for recovery. A sub-group of each treatment was taken every 24h, when MCN was scored in inflorescences and the levels of AA were determined in bracts. Ozone caused a significant increase in the frequency of MCN after 24-120 of recovery, compared to measurements in inflorescences from the control treatment, but maximal MCN rate was reached between 72 and 120 h of recovery. The highest percentages of MCN in both fumigation treatments were found during the winter experiment. Ozone exposure did not induce significant changes in the content of AA. However, it was positively influenced by daily amplitude of air temperature during the period of the bioassay. The intensity of genotoxic damage and the time lag necessary to visualize an enhanced number of MCN depended on the levels of ascorbic acid in bracts 24h before MCN scoring and on the daily amplitude of air temperature during the development of the bioassay. Narrower ranges between daily maximum and minimum temperatures (around 4 degrees C) during the days of experiment seemed to promote a more efficient diagnostic of genotoxiciy induced by ozone.


Assuntos
Micronúcleos com Defeito Cromossômico/efeitos dos fármacos , Ozônio/toxicidade , Tradescantia/efeitos dos fármacos , Poluentes Atmosféricos/toxicidade , Ácido Ascórbico/metabolismo , Flores/efeitos dos fármacos , Flores/genética , Flores/metabolismo , Modelos Lineares , Testes para Micronúcleos , Testes de Mutagenicidade , Oxidantes Fotoquímicos/toxicidade , Estações do Ano , Temperatura , Tradescantia/genética , Tradescantia/metabolismo
8.
Environ Monit Assess ; 138(1-3): 305-12, 2008 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-17616826

RESUMO

In Argentina no historical or present programs exist specifically assessing ecosystem health with respect to photochemical air pollution, although phytotoxic concentrations of near-ground ozone have been documented in recent years. Here we report our preliminary findings on field observations of ozone-like injury found in natural plant populations and agroecosystems late in the 2005 growing season in the Southern Hemisphere. Several possible ozone bioindicator plants which have not been previously documented were observed to exhibit foliar symptoms consistent with ozone-induced injury. Based on these results we intend to expand field surveys and complete the screening process for injury confirmation of the plant species described here. For this and future research we will be using controlled chamber studies based in the US. Continuous monitoring of tropospheric ozone does not currently take place in the region of central Argentina. The combined evidence provided by intermittent air quality sampling and the presence of ozone-like injury to vegetation indicates the need to establish air quality and ozone biomonitoring networks in this region.


Assuntos
Magnoliopsida/efeitos dos fármacos , Oxidantes Fotoquímicos/toxicidade , Ozônio/toxicidade , Argentina , Monitoramento Ambiental , Magnoliopsida/fisiologia , Folhas de Planta/efeitos dos fármacos , Folhas de Planta/fisiologia
9.
Environ Pollut ; 147(3): 446-53, 2007 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-17478022

RESUMO

The first report on oxidant-induced plant damage in the Valley of Mexico was presented over 30 years ago. Ozone is known to occur in the Mexico City Metropolitan Area and elsewhere as the cause of chlorotic mottling on pine needles that are 2 years old or older as observed in 1976 on Pinus hartwegii and Pinus leiophylla. Visible evidences for the negative effects of ozone on the vegetation of central Mexico include foliar injury expressed as chlorotic mottling and premature defoliation on pines, a general decline of sacred fir, visible symptoms on native forest broadleaved species (e.g. Mexican black cherry). Recent investigations have also indicated that indirect effects are occurring such as limited root colonization by symbiotic fungi on ozone-damaged P. hartwegii trees and a negative influence of the pollutant on the natural regeneration of this species. The negative ozone-induced effects on the vegetation will most likely continue to increase.


Assuntos
Poluentes Atmosféricos/toxicidade , Ozônio/toxicidade , Árvores/efeitos dos fármacos , Abies/efeitos dos fármacos , Exposição Ambiental/efeitos adversos , Monitoramento Ambiental/métodos , Eucalyptus/efeitos dos fármacos , Metais Pesados/toxicidade , México , Oxidantes Fotoquímicos/toxicidade , Material Particulado/toxicidade , Pinus/efeitos dos fármacos , Folhas de Planta/efeitos dos fármacos , Prunus/efeitos dos fármacos
10.
Ecotoxicol Environ Saf ; 63(2): 306-12, 2006 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-16677915

RESUMO

The effects induced by long-term (30 day) and short-term (6h) exposures to ozone on the physiological parameters in young plants of Caesalpinia echinata Lam., a Brazilian tree species, were determined. Potted plants were maintained in open-top chambers in Valencia, Spain, under charcoal filtered air (mean O3 level: 29 microg m3), nonfiltered air (NF; 43 microg m3), and nonfiltered air plus O3 (NF + O3; 68 microg m3), simulating prevailing concentrations observed in the city of São Paulo, Brazil, during spring months (50 microg m3 in 2002). In the plants kept in NF + O3 for 30 days, although no foliar visible injuries were observed, the net carbon assimilation rate was reduced to 50%, stomatal conductance 42%, and transpiration 40%, when compared to the results for the NF plants. No changes in antioxidants, in leaf, stem, and root biomass, and in the root/shoot ratio were observed. Significant reductions were observed in gas exchange and in PSII photochemical efficiency (Fv/Fm) after 6 h of exposure to an O3 peak. The species was shown to be sensitive to ambient O3 concentrations measured in São Paulo.


Assuntos
Caesalpinia/efeitos dos fármacos , Oxidantes Fotoquímicos/toxicidade , Ozônio/toxicidade , Ácido Ascórbico/metabolismo , Brasil , Caesalpinia/fisiologia , Fumigação , Peroxidases/metabolismo , Fotossíntese/efeitos dos fármacos , Folhas de Planta/efeitos dos fármacos , Folhas de Planta/crescimento & desenvolvimento , Folhas de Planta/metabolismo , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/crescimento & desenvolvimento , Brotos de Planta/efeitos dos fármacos , Brotos de Planta/crescimento & desenvolvimento , Caules de Planta/efeitos dos fármacos , Caules de Planta/crescimento & desenvolvimento , Transpiração Vegetal/efeitos dos fármacos , Superóxido Dismutase/metabolismo
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