Reactive oxygen species (ROS) are constantly generated as by-products of several physiological cellular processes or after toxic insults. To delay or prevent ROS-induced damage, cells have evolved antioxidant systems that convert free radicals into nontoxic form. Oxidative stress, which arises when ROS production exceeds their removal, is implicated in various disorders such as atherosclerosis, diabetes, cancer, aging, and neurodegeneration. The brain is believed to be particularly susceptible to ROS-induced damages, due to its reduced capacity for cellular regeneration. Oxidative stress seems to be involved in dopaminergic neuron degeneration observed in Parkinson's disease (PD).

Our aim is to analyze the potential protective role of superoxide dismutases (SODs) in cellular models that mimic dopaminergic neurons. Because of their ability to scavenge superoxide anion, SODs are considered the first line of defense against the downstream generation of more reactive ROS. In the present study, we generated stable cell lines overexpressing cytosolic and mitochondrial superoxide dismutases, SOD1 and SOD2, and we investigated their effects against toxic insults, related to PD, known to affect cell viability through ROS production. We observed a protective role exerted by SOD proteins that could be useful to define new therapeutic strategies against PD.