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Artículo

Reactive oxygen species produced by NADPH oxidase and mitochondrial dysfunction in lung after an acute exposure to Residual Oil Fly Ashes

Magnani, Natalia DanielaIcon ; Marchini, Timoteo OscarIcon ; Vanasco, VirginiaIcon ; Tasat, Deborah Ruth; Alvarez, SilviaIcon ; Evelson, Pablo AndresIcon
Fecha de publicación: 01/07/2013
Editorial: Elsevier
Revista: Toxicology and Applied Pharmacology
ISSN: 0041-008X
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Salud Pública y Medioambiental; Sistema Respiratorio

Resumen

Reactive O2 species production triggered by particulate matter (PM) exposure is able to initiate oxidative damage mechanisms, which are postulated as responsible for increased morbidity along with the aggravation of respiratory diseases. The aim of this work was to quantitatively analyse the major sources of reactive O2 species involved in lung O2 metabolism after an acute exposure to Residual Oil Fly Ashes (ROFAs). Mice were intranasally instilled with a ROFA suspension (1.0 mg/kg body weight), and lung samples were analysed 1 h after instillation. Tissue O2 consumption and NADPH oxidase (Nox) activity were evaluated in tissue homogenates. Mitochondrial respiration, respiratory chain complexes activity, H2O2 and ATP production rates, mitochondrial membrane potential and oxidative damage markers were assessed in isolated mitochondria. ROFA exposure was found to be associated with 61% increased tissue O2 consumption, a 30% increase in Nox activity, a 33% increased state 3 mitochondrial O2 consumption and a mitochondrial complex II activity increased by 25%. During mitochondrial active respiration, mitochondrial depolarization and a 53% decreased ATP production rate were observed. Neither changes in H2O2 production rate, nor oxidative damage in isolated mitochondria were observed after the instillation. After an acute ROFA exposure, increased tissue O2 consumption may account for an augmented Nox activity, causing an increased O2 •− production. The mitochondrial function modifications found may prevent oxidative damage within the organelle. These findings provide new insights to the understanding of the mechanisms involving reactive O2 species production in the lung triggered by ROFA exposure.
Palabras clave: Air Pollution , Lung , Mitochondria , Nadph Oxidase , Residual Oil Fly Ash (Rofa) , Reactive O2 Species
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/1910
URL: http://www.sciencedirect.com/science/article/pii/S0041008X1300135X
DOI: http://dx.doi.org/10.1016/j.taap.2013.04.002
Colecciones
Articulos(IBIMOL)
Articulos de INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR
Citación
Magnani, Natalia Daniela; Marchini, Timoteo Oscar; Vanasco, Virginia; Tasat, Deborah Ruth; Alvarez, Silvia; et al.; Reactive oxygen species produced by NADPH oxidase and mitochondrial dysfunction in lung after an acute exposure to Residual Oil Fly Ashes; Elsevier; Toxicology and Applied Pharmacology; 270; 1; 1-7-2013; 31-38
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