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Mitochondrial DNA variation and increased oxidative damage in euthymic patients with bipolar disorder
Author(s) -
Chang ChengChen,
Jou ShawHwa,
Lin TaTsung,
Liu ChinSan
Publication year - 2014
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/pcn.12163
Subject(s) - mitochondrial dna , oxidative stress , oxidative phosphorylation , dna damage , bipolar disorder , medicine , psychiatry , biology , dna , genetics , gene , biochemistry , lithium (medication)
Aim The aim of this study was to compare alterations of mitochondrial DNA (mt DNA ) copy number, single nucleotide polymorphisms, and oxidative damage of mt DNA in clinically stable patients with bipolar I disorder ( BD ). Methods Patients meeting DSM‐IV diagnostic criteria for BD were recruited from the psychiatric outpatient clinic at C hanghua C hristian H ospital, T aiwan. They were clinically stable and their medications had not changed for at least the preceding 2 months. Exclusion criteria were substance‐induced psychotic disorder, eating disorder, anxiety disorder or illicit substance abuse. Comparison subjects did not have any history of major psychiatric disorders and they were non‐smokers. By analyzing peripheral blood leukocytes, copy number, single nucleotide polymorphisms and oxidative damage of mt DNA were compared between the two groups. Results The median age of the subjects was 38 years and 41.5 years in the comparison and BD groups, respectively. The leukocyte mt DNA copy number of the BD group was significantly lower than that of the comparison group ( P < 0.001). BD patients had significantly higher mitochondrial oxidative damage than the comparison group (6.1 vs 3.9, P < 0.001). After generalized linear model adjusting with age, sex, smoking, family history, and psychotropic use, mt DNA copy number was still significantly lower in the BD group ( P < 0.001). MtDNA oxidative damage was positively correlated with age ( P = 0.034), although mt DNA oxidative damage was similar between these two groups. Conclusion Possible involvement of oxidative stress and mitochondria in the pathophysiology of BD needs more large‐scale studies. It is important that psychiatrists retain a high level of suspicion for mitochondrial dysfunction in patients with bipolar disorder.