Oxidative stress which results from an excessive accumulation of reactive oxygen species (ROS) has been implicated in a wide variety of human neurodegenerative diseases. The superoxide dismutases (SODs), catalase (CAT) and glutathione peroxidases (GPxs) play key roles in the cellular defense against ROS. Each one of this triad of enzymes has a specific function and each acts in concert with the others in the inactivation of ROS. The brain tissue appears to be especially vulnerable to oxidative stress, since it contains almost no catalase activity and has comparatively low levels of glutathione and GPx. Familial amyotrophic lateral sclerosis (fALS) which is a progressive degenerative disorder of motor neurons, is associated with deficiencies in SOD1 activity. On the other hand, in Down’s syndrome (DS) which resembles Alzheimer’s Disease (AD) in its final phases, SOD1 is overexpressed due to trisomy of chromosome 21. It appears, therefore, that both underexpression and overexpression of antioxidant enzymes may result in brain pathology.

 

In the present report, we review key published findings on the neurophysiological and neuropathological implications of imbalance in this group of antioxidant enzymes. In this context, we also present the results of some of our most recent experimental approaches using neurons in culture.