| First Author | Austin S | Year | 2011 |
| Journal | Free Radic Biol Med | Volume | 51 |
| Issue | 12 | Pages | 2243-8 |
| PubMed ID | 21964033 | Mgi Jnum | J:179298 |
| Mgi Id | MGI:5301757 | Doi | 10.1016/j.freeradbiomed.2011.08.036 |
| Citation | Austin S, et al. (2011) Impact of PGC-1alpha on the topology and rate of superoxide production by the mitochondrial electron transport chain. Free Radic Biol Med 51(12):2243-8 |
| abstractText | Reactive oxygen species (ROS) play an important role in normal signaling events and excessive ROS are associated with many pathological conditions. The amount of ROS in cells is dependent on both the production of ROS by the mitochondrial electron transport chain and their removal by ROS-detoxifying enzymes. The peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) is a master regulator of mitochondrial functions and a key regulator of the ROS-detoxifying program. However, the impact of PGC-1alpha on the topology and rate of superoxide production by the mitochondrial electron transport chain is not known. We report here, using mitochondria from muscle creatine kinase-PGC-1alpha transgenic mice, that PGC-1alpha does not affect the topology of ROS production, but increases the capacity of complexes I and III to generate ROS. These changes are associated with increased mitochondrial respiration and content of respiratory chain complexes. When normalizing ROS production to mitochondrial respiration, we find that PGC-1alpha preserves the percentage of free radical leak by the electron transport chain. Together, these data demonstrate that PGC-1alpha regulates the intrinsic properties of mitochondria in such a way as to preserve a tight coupling between mitochondrial respiration and ROS production. |
