The effects of ozone exposure and associated injury mechanisms on the central nervous system
Por:
Martínez-Lazcano J.C., González-Guevara E., Rubio, MD, Franco-Pérez J., Custodio V., Hernández-Cerón M., Livera C., Paz C.
Publicada:
1 jun 2013
Categoría:
Neuroscience (miscellaneous)
Resumen:
Ozone (O 3 ) 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 O 3 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 O 3 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 sleepwake cycle, neuronal dysfunctions, cell degeneration, and neurochemical alterations have also been described; furthermore, it has also been proposed that O 3 could have epigenetic effects. O 3 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 O 3 exposure is not well understood. In this review, the basic mechanisms of inflammation and activation of the immune system by O 3 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 O 3 exposure are discussed.
Filiaciones:
Martínez-Lazcano J.C.:
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, MVS Insurgentes Sur 3877, CP 14269 México, DF, Mexico
González-Guevara E.:
Univ Nacl Autonoma Mexico, Posgrad Ciencias Biol, Mexico City 04510, DF, Mexico
Franco-Pérez J.:
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, MVS Insurgentes Sur 3877, CP 14269 México, DF, Mexico
Custodio V.:
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, MVS Insurgentes Sur 3877, CP 14269 México, DF, Mexico
Hernández-Cerón M.:
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, MVS Insurgentes Sur 3877, CP 14269 México, DF, Mexico
Posgrado en Ciencias Farmacológicas, Universidad Autónoma Metropolitana, Calzada del Hueso 1100, CP 04960 México, DF, Mexico
Livera C.:
Univ Nacl Autonoma Mexico, Posgrad Ciencias Biol, Mexico City 04510, DF, Mexico
Paz C.:
Departamento de Neurofisiología, Instituto Nacional de Neurología y Neurocirugía, MVS Insurgentes Sur 3877, CP 14269 México, DF, Mexico
Posgrado en Ciencias Farmacológicas, Universidad Autónoma Metropolitana, Calzada del Hueso 1100, CP 04960 México, DF, Mexico
|