Increased oxidative stress in the anterior cingulate cortex of subjects with bipolar disorder and schizophrenia

Background:  Recent studies indicate the presence of mitochondrial dysfunction in brains of subjects with bipolar disorder (BD). Because the mitochondrial electron transport chain is a major source for production of reactive oxygen species that cause oxidative stress, we sought to determine in the p...

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Published in:Bipolar disorders 2009-08, Vol.11 (5), p.523-529
Main Authors: Wang, Jun-Feng, Shao, Li, Sun, Xiujun, Young, L Trevor
Format: Article
Language:English
Subjects:
4-hydroxynonenal
Aldehydes - metabolism
Analysis of Variance
bipolar disorder
Bipolar Disorder - pathology
Case-Control Studies
Depressive Disorder, Major - pathology
Female
Gyrus Cinguli - physiopathology
Humans
lipid peroxidation
Lipid Peroxidation - physiology
Male
mitochondrial dysfunction
Oxidative Stress - physiology
Postmortem Changes
postmortem cingulate cortex
Schizophrenia - pathology
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Summary:Background:  Recent studies indicate the presence of mitochondrial dysfunction in brains of subjects with bipolar disorder (BD). Because the mitochondrial electron transport chain is a major source for production of reactive oxygen species that cause oxidative stress, we sought to determine in the present study if BD is associated with oxidative stress. Methods:  Postmortem anterior cingulate brain sections from subjects with BD, major depressive disorder (MDD), or schizophrenia, and from nonpsychiatric, non‐neurologic comparison controls were generously provided by the Stanley Foundation Neuropathology Consortium. Oxidative stress was determined by analyzing 4‐hydroxynonenal (4‐HNE), a major product of lipid peroxidation. The level of 4‐HNE was determined by measuring 4‐HNE protein adducts using immunohistochemistry. Results:  We found that 4‐HNE levels were significantly increased by 59% in BD subjects and by 47% in schizophrenia subjects, but not in MDD subjects, when compared with controls. Levels of 4‐HNE were negatively correlated with pH in all 60 subjects. When pH was used as covariate, 4‐HNE levels were still significantly increased in BD subjects when compared with controls. Further, 4‐HNE levels were significantly correlated with pH values only in BD subjects, but not in MDD, schizophrenia, or control subjects. Conclusions:  Oxidative damage in the brain may contribute in part to the pathological process in BD and schizophrenia. This finding also suggests antioxidative stress as a probable alternative approach to the pharmacological treatment of these psychiatric disorders.
ISSN:1398-5647
1399-5618
DOI:10.1111/j.1399-5618.2009.00717.x