Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may
lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to
oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and
activities of enzymatic and antioxidant systems in schizophrenia.
Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in
schizophrenia pathology due to oxidative stress, particularly lipid peroxidation.
Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus
region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances
(TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also
Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy
control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of
schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ±
1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated
TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects
an increased lipid peroxidation (LPO).
Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of
schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production.
Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative
stress in schizophrenia pathology.