RESUMEN
There is an increased concern about the health effects that air-suspended particles have on human health which have been dissected in animal models. Using CD-1 mouse, we explore the effects that vanadium inhalation produce in different tissues and organs. Our findings support the systemic effects of air pollution. In this paper, we describe our findings in different organs in our conditions and contrast our results with the literature.
Asunto(s)
Contaminación del Aire/efectos adversos , Material Particulado/toxicidad , Vanadio/toxicidad , Animales , Huesos/efectos de los fármacos , Huesos/patología , Sistema Nervioso Central/efectos de los fármacos , Sistema Nervioso Central/patología , Roturas del ADN de Cadena Simple , Humanos , Sistema Inmunológico/patología , Inhalación , Hígado/efectos de los fármacos , Hígado/patología , Pulmón/efectos de los fármacos , Pulmón/patología , Ganglios Linfáticos/efectos de los fármacos , Ganglios Linfáticos/patología , Ratones , Modelos Animales , Especies Reactivas de Oxígeno/metabolismo , Reproducción/efectos de los fármacos , Bazo/efectos de los fármacos , Bazo/patologíaRESUMEN
Olfactory dysfunction is a common symptom reported by patients with neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. Despite the knowledge gathered about the pathology of these diseases, little information has been generated regarding the ultrastructure modifications of the granule cells that regulate the information for odor identification. Swollen organelles and nuclear invaginations identified the exposed mice. Necrosis was evidenced at 4th week of exposure, whereas apoptosis arose at 8th week of exposure. A ruffled electron-dense membrane changes were also found. The changes observed could be explained by the reactive oxygen species generated by manganese and its effects on the membrane's structure and on the cytoskeleton's function. This study contributes to correlate metal air pollution and neurodegenerative changes with olfactory affection.
Asunto(s)
Manganeso/toxicidad , Neuronas/patología , Trastornos del Olfato/inducido químicamente , Trastornos del Olfato/patología , Bulbo Olfatorio/efectos de los fármacos , Contaminación del Aire/efectos adversos , Animales , Cloruros/toxicidad , Exposición por Inhalación , Masculino , Compuestos de Manganeso , Ratones , Necrosis , Degeneración Nerviosa , Neuronas/ultraestructura , Orgánulos/ultraestructuraRESUMEN
The present study investigates the effects of divalent and trivalent manganese (Mn(2+)/Mn(3+)) mixture inhalation on mice to obtain a novel animal model of Parkinson disease (PD) inducing bilateral and progressive cell death in the substantia nigra compacta (SNc) and correlating these alterations with motor disturbances. CD-1 male mice inhaled a mixture of 0.04 M manganese chloride (MnCl(2)) and manganese acetate (Mn(OAc)(3)), 1 h twice a week for 5 months. Before Mn exposure, animals were trained to perform motor function tests and were evaluated each week after the exposure. By doing this, overall behavior was assessed by ratings and by videotaped analyses; by the end of Mn exposure period, animals were killed. The mesencephalon was processed for tyrosine hydroxylase (TH) immunocytochemistry. After 5 months of Mn mixture inhalation, mice developed evident deficits in their motor performance manifested as akinesia, postural instability and action tremor. SNc of the Mn-exposed animals showed an important decrease (67.58%) in the number of TH-immunopositive neurons. Our data provide evidence that MnCl(2) and Mn(OAc)(3) mixture inhalation produces similar morphological and behavioral alterations to those observed in PD providing a useful experimental model for the study of this neurodegenerative disease.
Asunto(s)
Acetatos/toxicidad , Conducta Animal/efectos de los fármacos , Cloruros/toxicidad , Modelos Animales de Enfermedad , Exposición por Inhalación , Compuestos Organometálicos/toxicidad , Enfermedad de Parkinson , Animales , Relación Dosis-Respuesta a Droga , Conducta Alimentaria/efectos de los fármacos , Masculino , Compuestos de Manganeso , Ratones , Actividad Motora/efectos de los fármacos , Enfermedad de Parkinson/etiología , Enfermedad de Parkinson/metabolismo , Enfermedad de Parkinson/patología , Desempeño Psicomotor/efectos de los fármacos , Sustancia Negra/metabolismo , Sustancia Negra/patología , Factores de Tiempo , Tirosina 3-Monooxigenasa/metabolismoRESUMEN
Vanadium (V) derivatives are well-known environmental pollutants and its toxicity has been related with oxidative stress. Toxicity after vanadium inhalation on the substantia nigra, corpus striatum, hippocampus and ependymal epithelium was reported previously. The purpose of this study was to analyse the role of matrix metalloproteinases 2 (MMP-2) and 9 (MMP-9) in the changes observed in brain tissue after chronic V inhalation. Mice were exposed to vaporized, vanadium pentoxide 0.02 m in deionized water for 1 h twice a week, and killed at 1 h, 1, 2 and 4 weeks after exposure. The brain was removed and the olfactory bulb, prefrontal cortex, striatum and hippocampus were dissected and the MMP content was obtained by zymography. The results showed that MMP-9 increased in all the structures at the end of the exposure, although in the hippocampus this increment was evident after 1 week of exposure. When MMP-2 was analysed in the olfactory bulb and prefrontal cortex it remained unchanged throughout the whole exposure, while in the hippocampus it increased at week 4, while in the striatum MMP-2 increased from the second week only, through the whole experiment. These results demonstrate that V increased MMPs in different structures of the CNS and this change might be associated with the previously reported modifications, such as dendritic spine loss and neuronal cell death. The modifications in MMPs could be related with blood-brain barrier (BBB) disruption which was reported previously. Oxidative stress might also be involved in the activation of these gelatinases as part of the different mechanisms which take place in V toxicity in the CNS.
Asunto(s)
Sistema Nervioso Central/efectos de los fármacos , Sistema Nervioso Central/enzimología , Metaloproteinasa 2 de la Matriz/metabolismo , Metaloproteinasa 9 de la Matriz/metabolismo , Vanadio/toxicidad , Administración por Inhalación , Animales , Encéfalo/efectos de los fármacos , Encéfalo/enzimología , Química Encefálica/efectos de los fármacos , Densitometría , Electroforesis en Gel de Poliacrilamida , Masculino , Ratones , Estrés Oxidativo/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismo , Vanadio/administración & dosificaciónRESUMEN
The interaction of ozone with some molecules results in an increased production of free radicals. The objective of this study was to identify whether acute ozone exposure to 1-1.5 ppm for 4 h, produced cytological and ultrastructural modifications in the olfactory bulb cells. The results showed that in rats exposed to ozone there was a significant loss of dendritic spines on primary and secondary dendrites of granule cells, whereas the control rats did not present such changes. Besides these exposed cells showed vacuolation of neuronal cytoplasm, swelling of Golgi apparatus and mitochondrion, dilation cisterns of the rough endoplasmic reticulum. These findings suggest that oxidative stress produced by ozone induces alterations in the granule layer of the olfactory bulb, which may be related to functional modifications.
Asunto(s)
Dendritas/efectos de los fármacos , Bulbo Olfatorio/efectos de los fármacos , Ozono/toxicidad , Animales , Dendritas/ultraestructura , Radicales Libres , Exposición por Inhalación , Masculino , Microscopía Electrónica , Bulbo Olfatorio/ultraestructura , Orgánulos/efectos de los fármacos , Orgánulos/ultraestructura , Ozono/administración & dosificación , Ratas , Ratas WistarRESUMEN
Exposure to ozone results in an increased production of free radicals which causes oxidative stress. The purpose of this study was to determine the effects of ozone exposure on memory and its correlation with the cytology of the hippocampus. Twenty-four male Wistar rats were exposed to 1 ppm (parts per million) ozone for 4 h in a closed chamber. Control group was exposed to flowing air. After ozone exposure, the rats were given long-term (24 h) memory training which consists of a passive avoidance conditioning. After that the animals were perfused and the brains were placed in the Golgi stain. The analysis consisted in counting the dendritic spines in five secondary and five tertiary dendrites of each of the 20 pyramidal neurons of hippocampus CA1 analyzed. Our results showed alterations on long-term memory and a significant reduction of dendritic spines, and provided evidence that this deterioration in memory is probably due to the reduction in spine density in the pyramidal neurons of hippocampus.