All mutations impairing mitochondrial dynamics result in severe diseases mostly of the neuronal system. Thus the question arises how the continuous fusion and division processes, the generation and degradation of mitochondria contribute to the wellbeing of a cell. Mitochondria are the main source for reactive oxygen species (ROS) which primarily have an impact on the mitochondria themselves. Depending on the proliferative state of cells dysfunctional parts of mitochondria might be eliminated via fission processes followed by mitophagy or by dilution taking place in huge mitochondrial networks by shifting the morphological equilibrium to fusion. A process which conveys resistance to the chondriome against the damaging influences of ROS. The mechanisms which support survival of mitochondria in a hostile environment differ with the severeness of ROS impact and with age of the cells. This is exemplified in models for selective impairment of mitochondrial function via phototoxicity in human umbilical vein endothelial cells, either young and proliferative or in the state of proliferative senescence. The different rescue pathways are controlled by expression of genes coding for proteins related to fusion and fission and those involved in autophagy. Mitochondrial membrane potential and morphology, cellular ATP-content, integrity of mtDNA, ROS content and ROS-resistance prove the significance of the different pathways.