RESUMO
Ozone exposure induces increased production of free radicals which may result in oxidative stress. The objectives of this study were to determine the antioxidant effects of vitamin E on memory deficits and lipid peroxidation due to oxidative stress caused by acute ozone exposure. Rats were exposed to 0.7 p.p.m. ozone for 4 h and 50 mg/kg vitamin E was administered either before or after exposure. Experiment 1 evaluated alterations in short-term and long-term memory in a passive avoidance task. Experiment 2 quantified lipid peroxidation levels of the striatum, hippocampus and frontal cortex. Vitamin E administered before or after ozone exposure blocked memory deterioration and increases in lipid peroxidation levels associated with oxidative stress.
Assuntos
Antioxidantes/farmacologia , Peroxidação de Lipídeos/efeitos dos fármacos , Transtornos da Memória/psicologia , Oxidantes Fotoquímicos , Ozônio , Vitamina E/farmacologia , Animais , Aprendizagem da Esquiva/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Masculino , Memória/efeitos dos fármacos , Transtornos da Memória/induzido quimicamente , Atividade Motora/efeitos dos fármacos , Neostriado/efeitos dos fármacos , Neostriado/metabolismo , Estresse Oxidativo , Córtex Pré-Frontal/efeitos dos fármacos , Córtex Pré-Frontal/metabolismo , Ratos , Ratos WistarRESUMO
The purpose of this study was to analyze the possible morphological recovery of the granule cells in the olfactory bulb as a consequence of oxidative stress after an acute ozone exposure. Rats were divided in two groups: Control (air exposed) and experimental group, exposed 4 h, to 1 ppm ozone and divided into 4 subgroups, which were sacrificed at 2 and 24 h, 10 and 15 days, respectively. Olfactory bulbs were processed with the rapid Golgi method and for transmission electron microscopy. The granule cells of the olfactory bulb disclosed less dendritic spine density at 2, 24 h, and 10 days after the exposure compared with controls. At 15 days, the number of spines increased to values similar to those found in controls. The granule cells ultrastructure demonstrated an increment in lipofucsin granules, as well as swollen organelles, changes that decreased overtime. This change decline might be related to a partial recovery of the associative granule cells function.
Assuntos
Bulbo Olfatório/citologia , Bulbo Olfatório/efeitos dos fármacos , Oxidantes Fotoquímicos/toxicidade , Ozônio/toxicidade , Animais , Masculino , Microscopia Eletrônica de Transmissão , Neurônios/efeitos dos fármacos , Neurônios/ultraestrutura , Estresse Oxidativo , Ratos , Ratos Wistar , Recuperação de Função Fisiológica , Vacúolos/ultraestruturaRESUMO
Ozone is one of the main atmospheric pollutants. Its inhalation causes an increase in free radicals, when these free radicals are not compensated by antioxidants, it leads to an oxidative stress state. This oxidative stress state has been implicated in neurodegenerative processes. To determine the effects of oxidative stress caused by exposure to ozone on memory and motor activity, we used 120 male Wistar rats exposed to one of the following ozone doses, (0.0, 0.1, 0.4, 0.7, 1.1 and 1.5 ppm), for four hours. After ozone exposure, short and long term memory of a one trial passive avoidance test were measured, and motor activity was registered for five minutes, in 10 rats of each group. In 16 rats exposed to 0.0, 0.4, 0.7 or 1.1 ppm lipid peroxidation levels from frontal cortex, hippocampus, striatum and cerebellum, were measured. Results show that ozone, causes memory impairment from doses of 0.7 ppm, decrease in motor activity from doses of 1.1 ppm, and increase in lipid peroxidation levels from doses of 0.4 ppm. that increase with the dose.
Assuntos
Peroxidação de Lipídeos/efeitos dos fármacos , Memória/efeitos dos fármacos , Atividade Motora/efeitos dos fármacos , Ozônio/farmacologia , Animais , Comportamento Animal/efeitos dos fármacos , Química Encefálica , Condicionamento Operante/fisiologia , Peróxidos Lipídicos/análise , Masculino , Ratos , Ratos WistarRESUMO
To determine the antioxidant effects of taurine on changes in memory and lipid peroxidation levels in brain caused by exposure to ozone, we carried out two experiments. In the first experiment, 150 rats were separated into three experimental blocks (young, mature, and old) with five groups each and received one of the following treatments: control, taurine, ozone, taurine before ozone, and taurine after ozone. Ozone exposure was 0.7-0.8 ppm for 4 h and taurine was administered ip at 43 mg/kg, after or before ozone exposure. Subsequently, rats were tested in passive avoidance conditioning. In the second experiment, samples from frontal cortex, hippocampus, striatum, and cerebellum were obtained from 60 rats (young and old), using the same treatments with 1 ppm ozone. Results show both an impairment in short-term and long-term memory with ozone and an improvement with taurine after ozone exposure, depending on age. In contrast to young rats, old rats showed peroxidation in all control groups and an improvement in memory with taurine. When taurine was applied before ozone, we found high peroxidation levels in the frontal cortex of old rats and the hippocampus of young rats; in the striatum, peroxidation caused by ozone was blocked when taurine was applied either before or after ozone exposure.