Wood smoke exposure induces a decrease in respiration parameters and in the activity of respiratory complexes I and IV in lung mitochondria from guinea pigs.

Abstract:

: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 O2 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.

journal_name

Environ Toxicol

journal_title

Environmental toxicology

authors

Granados-Castro LF,Rodríguez-Rangel DS,Montaño M,Ramos C,Pedraza-Chaverri J

doi

10.1002/tox.21922

subject

Has Abstract

pub_date

2015-04-01 00:00:00

pages

461-71

issue

4

eissn

1520-4081

issn

1522-7278

journal_volume

30

pub_type

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