Journal
ENVIRONMENTAL TOXICOLOGY
Volume 30, Issue 4, Pages 461-471Publisher
WILEY-BLACKWELL
DOI: 10.1002/tox.21922
Keywords
wood smoke; mitochondrial respiration; chronic obstructive pulmonary disease; respiratory complexes
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Funding
- Consejo Nacional de Ciencia y Tecnologia (CONACYT) [129838]
- Programa de Apoyo a Proyectos de Investigacion (PAPIIT) [IN210713]
- Apoyo del recurso asignado al INER gestionado en la LXI Legislaturas de la Camara de Diputados, a traves de su Comision de Equidad y Genero, para la asignacion presupuestal para la Atencion de las Enfermedades Asociadas al Uso de Lena en
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Domestic exposure to biomass smoke represents the second cause of chronic obstructive lung disease. Previous studies have shown that exposure of guinea pigs to wood smoke is capable of generating oxidative stress in lung tissue, and this may involve a failure at a mitochondrial level, given its close relation with the production of reactive oxygen species (ROS). The purpose of this study was to evaluate, in guinea pigs exposed to wood smoke, the lung mitochondrial functionality through O-2 consumption measurement and the determination of the mitochondrial complexes enzymatic activity. We found that normal and maximum respiration decreased at 15 and 30 min of wood smoke exposure, recovering its normal values at 180 min. The same behavior was observed for the respiratory control rate (RCR) and the ADP/O value. Complex I activity decreased significantly after 30 min of exposure and it returned to baseline after 180 min. The greatest alteration was observed by the decrease of 85% on complex IV activity at 30 min of exposure, which returned to control values after 180 min of exposure. It is concluded that even when wood smoke exposure induces severe mitochondrial respiration alterations at the first 30 min, it seems that there is one or many ways by which mitochondria can reinstate its normal function after 180 min of exposure. (c) 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 461-471, 2015.
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