Catalase to Reduce Mitochondrial Oxidative Stress Does Not Reduce Cellular Senescence

Every cell contains hundreds of mitochondria, the descendants of ancient symbiotic bacteria now integrated into the cell. Mitochondria generate oxidative molecules as a consequence of the processes that generate the chemical energy store molecule adenosine triphosphate (ATP), used to power the cell. Those oxidative molecules cause damage, near all rapidly repaired. They also serve as signals, such as in the beneficial response to exercise. With aging, however, mitochondrial function becomes impaired and the degree of oxidative stress generated by the operation of mitochondria becomes harmful. Researchers have in the past produced modestly extended life in short-lived model organisms by overexpression of natural mitochondrial antioxidants such as catalase or via use of engineered antioxidant molecules targeted to mitochondria like SkQ1. This approach of dampening excessive mitochondrial generation of oxidative molecules seems generally beneficial, but the effects on life span in mice are small in more recent, more rigorously conducted studies. Today's open access paper provides a further data point, in that the scientists involved demonstrate that catalase upregulation fails to reduce the burden of cellular senescence in old mice. As they point out, this somewhat complicates present thinking on the interactions between age-related mitochondrial dysfunction and burden of cellular senescence. Mitochondria-Targeted Catalase Does Not Suppress Development of Cellular ...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs