Abstract
Airborne particulate matter (PM10) has potential adverse health effects in human, especially in lung tissue and those effects are related to an increase in several diseases and cancer. We have previously demonstrated that PM10 increases reactive oxygen species (ROS) formation, decrease in antioxidant enzymes activity and these effects are observed under sub-lethal conditions. In this regard, mitochondria are the main source of ROS but little is known about alterations induced in mitochondrial function after PM10 exposure. We hypothesized that if PM10 induces an increase in ROS generation, it could be possible to find alterations mitochondrial function. To test our hypothesis we exposed enriched mitochondria preparations from lung tissue of rat for 1 hour to the following PM10 concentrations: 1, 5, 10, 30 and 50 μg/mL. We measured the oxygen consumption after PM10 exposure using a Clark type electrode and also the activity of mitochondrial complexes. In addition, the mitochondrial membrane potential was determined by rhodamine 123 staining using confocal microscopy. Our results showed a decrease in the respiratory control index and ADP phosphorylation over 50%, a decrease in the activity of complex IV and an important decrease in mitochondrial membrane potential. In conclusion, PM10 induces a decrease in oxygen consumption, ADP phosphorylation and loss of mitochondrial membrane potential. These effects are related to the decrease in activity of complex IV. Our research will be guided to investigate if the mitochondrial alterations induced by PM10 exposure could be related to mitochondrial dysfunction and metabolic alterations found in cancer cells.
- © 2011 ERS
