OXIDATIVE INJURY AND POTENTIAL USE OF ANTIOXIDANTS IN SCHIZOPHRENIA

There is increasing evidence that oxidative injury contributes to path ophysiology of schizophrenia, indicated by the increased lipid peroxid ation products in plasma and CSF, and altered levels of both enzymatic and non-enzymatic antioxidants in chronic and drug-naive first-episod e schizophrenic patients. The increased plasma lipid peroxidation is a lso supported by concomitant lower levels of esterified polyunsaturate d essential fatty acids of red blood cell plasma membrane phospholipid s. Because membrane phospholipids play a critical role in neuronal sig nal transduction, oxidative damage of these lipids may contribute to t he proposed altered neurotransmitter receptor-mediated signal transduc tion and thereby alter information processing in schizophrenia. Adjunc tive treatment with antioxidants (e.g. vitamins E and C, beta-carotene and quinones) at the initial stages of illness may prevent further ox idative injury and thereby ameliorate and prevent further possible det erioration of associated neurological and behavioral deficits in schiz ophrenia.