Over-expression of the mitochondrial superoxide dismutase (PaSOD3) leads to alterations of lifespan, protein quality control and ROS scavenging system

Within biological systems, reactive oxygen species are formed as by-products of electron transport processes. Due to their ability to damage cellular compounds, ROS are central components of the ‘free radical theory of aging'. Fortunately, all biological systems have evolved various pathways to deal with this harmful situation. One of these pathways is the enzymatic ROS scavenging system in which superoxide dismutases (SODs) play an important role.

The fungal aging model Podospora anserina contains three SODs in different cellular compartments. In order to investigate the effect of altered mitochondrial SOD abundance and activity in P. anserina, we generated a deletion and three independent over-expression strains of PaSod3. While deletion of PaSod3 leads to decreased paraquat resistance, sensitivity against hydrogen peroxide and lifespan are not significantly changed when compared to the wild-type strain. In contrast, over-expression of PaSod3 leads to lifespan reduction and increased sensitivity against oxidative stress. The negative effects of the PaSod3 over-expression are correlated with a strong reduction in the abundance of mitochondrial peroxiredoxin and a matrix protease disclosing impairments of ROS scavenging pathway and mitochondrial quality control.

Recently we found that the catalase activity of PaCATB seems to be up-regulated in PaSod3 over-expression strains suggesting that the over-expressors have an increased hydrogen peroxide level.