Abstract
Research on the complex and multifaceted nature of Bipolar Disorder (BD) pathophysiology has recently expanded to include oxidative stress. Several lines of evidence have reported higher reactive oxygen species production that results in increased oxidative damage in proteins, lipids, and nucleic acids. These findings have been observed in brains and peripheral samples of BD patients, as well as being reproduced in a number of animal model studies. Also discussed in this review is research highlighting antioxidant properties of existing mood stabilizing drugs, with consideration paid to novel therapeutic treatments for BD through the alleviation of oxidative stress. The maladaptive oxidative modifications of cellular macromolecules may be associated with impaired neuroplasticity and the development of functional abnormalities in the brain.
Highlights
Bipolar Disorder (BD) is a severe psychiatric illness characterized by cycling episodes of mania and depression
In 2009, Wang et al [12] reported that 4-hydroxynonenal (4-HNE) protein adducts are significantly increased in postmortem Anterior Cingulate Cortex (ACC) of subjects diagnosed with either BD or schizophrenia when compared to nonpsychiatric populations
Studies have reported that repeated amphetamine administration was associated with increases in superoxide production [38], and protein and lipid oxidative damage in rat brain [39], with longer periods of exposure being positively correlated with oxidative stress
Summary
Bipolar Disorder (BD) is a severe psychiatric illness characterized by cycling episodes of mania and depression. Oxidative stress can occur through overproduction of free radicals or decrease in antioxidant defense systems or through both at once These free radicals can cause substantial damage to macromolecules through the generation of adducts, destruction of unsaturated C-C bonds, and oxidation of disulfides [8]. When kept in controlled conditions by antioxidant systems; free radicals can serve important functions in physiological processes [9] They are continuously produced in vivo by all tissues of the body, primarily during oxidative phosphorylation in the mitochondria. In BD, accumulating evidence from a range of studies using post-mortem brain tissue and peripheral blood samples has demonstrated increased oxidative damage to cellular macromolecules These studies have demonstrated a decrease in antioxidant capacity. Relevant to current and future development of therapeutics, there have been numerous reports of mood-stabilizing drugs producing neuroprotective effects against oxidative damage and increased antioxidant expression and activity
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