®®®® SIIA Público

Título del libro: Ozone And Ozone Depletion: Sources, Environmental Impact And Health
Título del capítulo: Systemic inflammation and neuronal dysfunction produced by ozone exposure

Autores UNAM:
CARLOS HERLINDO PAZ TRES;
Autores externos:

Idioma:
Inglés
Año de publicación:
2012
Palabras clave:

Cytokines; Neuroinflammation; Ozone


Resumen:

Ozone (O3), the major component of air pollution has a significant impact on public health. Besides the described effects on inflammation of the airways, there are many evidences indicating that exposure to O3 affects the central nervous system (CNS). The biological effects of O3 are attributed to their ability to cause oxidation and peroxidation of biomolecules directly and/or via free radical reactions, which in turn generates pathological damage to the respiratory system and extra pulmonary effects. The initial concentration and the maximum doses of O3 in tissues occur in the nose and the surfactant barrier although other effects are localized in the terminal bronchioles and alveolar ducts where the injured membrane generate aldehydes such malondialdehyde, 9 hidroxy-nonenal and other products of reaction of O3 with unsaturated lipids of membrane and induce the expression of factors such as cytokines, reactive oxygen species (ROS), reactive nitrogen species (RNS) which are secreted into the blood. The augmented production of pro-inflammatory products released from injured membranes has been evidenced mainly by the increase of lipid ozonation products (LOP), arachidonic acid (AA), leukotrienes, tromboxanes, TNF-a, IL-1ß the Nrf2 and NF-?B transcription factors. All these factors can induce the loss of cells and inflammatory processes in the lung, heart and liver. The loss cells involve the activation and proliferation of neutrophils and macrophages that propagate the effect to other organs including the tissue nearest to the blood-brain barrier (BBB). Furthermore, the activation of inflammatory cells near to BBB produce damage into the BBB and increase proinflammatory molecules transported across to the BBB into the brain, producing oxidative stress and neuroinflammation. These processes can induce several brain alterations including neurodegeneration. In this review we described the signaling pathways activated as consequence of the environmental exposition to O3 and their effects on nervous system which produce changes in learning, memory and altered motor activity. © 2013 Nova Science Publishers, Inc. All rights reserved.


Entidades citadas de la UNAM: