Defects of mitochondrial electron transport chain in bipolar disorder: implications for mood-stabilizing treatment.
OBJECTIVE
Converging lines of evidence indicate that defects in the mitochondrial electron transport chain (ETC) are associated with bipolar disorder (BD), and that mood-stabilizing drugs produce neuroprotective effects. Our objective is to review the most recent findings regarding this research.


METHODS
We searched MEDLINE and have reviewed here the most recently published articles.


RESULTS
There are deletions, mutation, and decreased expression of mitochondrial ETC complexes in BD. Because ETC is a major source of reactive oxygen species, these factors, along with decreased expression of antioxidant enzymes in BD, suggest the presence of oxidative damage in this disorder. Numerous recent studies have shown that mood-stabilizing drugs produce neuroprotective effects against oxidative damage and increase expression and activities of endogenous antioxidant enzymes in the rat brain.


CONCLUSIONS
These findings indicate that the process of oxidative damage could be a significant therapeutic target for the treatment of BD with mood-stabilizing drugs.
Wang
Jun-Feng
JF
Department of Psychiatry, University of British Columbia, Vancouver. junfengw@exchange.ubc.ca
D018692:Antimanic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001714:Bipolar Disorder / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology*; D045222:Electron Transport Chain Complex Proteins / Q000235:genetics / Q000502:physiology*; D006801:Humans; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species
D018692:Antimanic Agents; D000975:Antioxidants; D045222:Electron Transport Chain Complex Proteins; D017382:Reactive Oxygen Species