ROS production is proportional to the increase in mitochondrial respiration and electron chain activity. Numerous factors (including radiations, oxygen shortage, carcinogens and inflammation) can give rise to ROS, ultimately leading to ROS- mediated genomic instability and cancer. Under normal conditions, the balance between ROS levels are tightly controlled by an inducible antioxidant program that responds to cellular stressor, including enzymes such as superoxide dismutase, catalase, and those involved in glutathione metabolism. Some components of the ROS scavenging pathway are linked to mitochondrial oxidative metabolism by the PGC-l coactivators that enable cells to maintain normal redox status in response to changing oxidative capacity. The increase in mitochondrial number stimulated by these proteins could cause an increase in the production of ROS. Therefore, if ROS production were proportional to the increase of electron transport activity stimulated by the PGC-l proteins, these molecules would ultimately drive ROS levels higher. However, PGC-la is able to upgrade aerobic energy metabolism in tissues with high aerobic demand promoting ROS formation on one hand and ROS scavenging .systems on the other. Since the role of PGC-l ß in this process is completely unknown and ROS production is .commonly linked to mitochondrial dysfunctions that, in turn, are linked with several diseases, such as intestinal cancer and several metabolic diseases including steatohepatitis, we decided to investigate whether PGC-l ß could be involved in the mitochondrial homeostasis and ROS generation in two different organs, the intestine and the liver.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:578563 |
| Date | January 2011 |
| Creators | Bellafante, Elena |
| Publisher | Open University |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
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