**4. Conclusion**

The biochemical characteristics and physiology of the CNS strongly suggest that the brain is susceptible to oxidative damage and that oxidative stress is part of the pathophysiological mosaic of numerous neurological and psychiatric diseases. More importantly, oxidative stress is one of several biochemical mechanisms responsible for neurodegeneration in mental disorders, which can be limited as in schizophrenia, bipolar disorder, and depression, or reflected in massive apoptosis as in Alzheimer's disease. As the primary enzyme of antioxidant protection, SOD plays a significant role in preventing amplification of oxidative stress, production of more toxic free radicals and initiation of the internal apoptosis pathway. Although the results are inconsistent, in most studies the activity of SOD in major psychiatric illnesses has been altered. The inconsistency of the results may be a consequence of the heterogeneity of the disorders themselves, testing at different stages of the disease or the influence of psychopharmaceuticals on the enzyme activity and expression. In view of all the above, modulation of SOD activity can be considered in the light of a potential therapeutic target in major psychiatric illnesses.
