10.6084/m9.figshare.8117969.v1
Piotr Czarny
Piotr
Czarny
Paulina Wigner
Paulina
Wigner
Justyna Strycharz
Justyna
Strycharz
Ewa Swiderska
Ewa
Swiderska
Ewelina Synowiec
Ewelina
Synowiec
Magdalena Szatkowska
Magdalena
Szatkowska
Agnieszka Sliwinska
Agnieszka
Sliwinska
Monika Talarowska
Monika
Talarowska
Janusz Szemraj
Janusz
Szemraj
Kuan-Pin Su
Kuan-Pin
Su
Michael Maes
Michael
Maes
Tomasz Sliwinski
Tomasz
Sliwinski
Piotr Galecki
Piotr
Galecki
Mitochondrial DNA copy number, damage, repair and degradation in depressive disorder
Taylor & Francis Group
2019
Depression
mitochondrial DNA damage
mitochondrial DNA copy number
mitochondrial DNA repair
mitochondrial DNA degradation
2019-05-13 09:33:42
Journal contribution
https://tandf.figshare.com/articles/journal_contribution/Mitochondrial_DNA_copy_number_damage_repair_and_degradation_in_depressive_disorder/8117969
<p><b>Objectives:</b> We aimed to explore mitochondrial DNA (mtDNA) copy number, damage, repair and degradation in peripheral blood mononuclear cells (PBMCs) of patients with depression and to compare the results with healthy subjects.</p> <p><b>Methods:</b> Total genomic DNA was isolated from PBMCs of 25 depressed and 60 healthy subjects before, immediately after, and 3 h after the exposure to H<sub>2</sub>O<sub>2</sub>. Evaluation of mtDNA copy number was performed using real-time PCR and 2-ΔCt methods. Semi-long run real-time PCR was used to estimate the number of mtDNA lesions.</p> <p><b>Results:</b> Baseline mtDNA copy number did not differ in cells of healthy and depressed subjects; however, it was negatively correlated with the severity of the episode. After a 10-min challenge with hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), depressed patients’ PBMCs exhibited slower changes of the copy number, indicating a lower efficiency of mtDNA degradation compared to controls. Moreover, a significantly higher number of mtDNA lesions was found in depressed patients at the baseline as well as at other experimental time points. mtDNA lesions were also elevated in depressed patient cells immediately after H<sub>2</sub>O<sub>2</sub> exposure. Induction of oxidative stress had no significant influence on the cells of controls.</p> <p><b>Conclusions:</b> We are the first to show that impairment in repair and degradation of mtDNA may be involved in the pathophysiology of depression.</p>