In the filamentous fungus Podospora anserina, mitochondrial oxidative stress is a major contributor to aging. Reactive oxygen species (ROS) generated as a result of electron leakage during respiration lead to damage of components of the electron transport chain. In aging wild-type cultures, damaged proteins cannot be replaced because the mitochondrial genes encoding some of the corresponding subunits gradually become deleted from the mitochondrial DNA (mtDNA). Consequently, these defects result in an increased generation of reactive oxygen species and respiration deficits leading to cell death. Analyses of wild-type strains and of different long-lived mutants of P. anserina provide strong evidence that molecular mechanisms controlling aging processes in this fungus are complex and act at different levels. A basic mechanism (e.g., damage by ROS) appears to be overlaid by prominent instabilities of the mtDNA.