The association of DNA damage and repair with symptomatic and remitted states of depression

Introduction: Presence of higher risk for medical comorbidity, cognitive impairments and mortality in depression suggests a central role of DNA damage/repair mechanisms in etiopathogenesis of depression. The aim of the study was to determine the relationship between DNA damage/repair and the depressive symptoms, symptom severity and symptomatic remission in depression. Methods: Thirty three unipolar depression, 24 bipolar depression and 61 healthy volunteers were included in the study. In the first visit, diagnostic interviews and clinical assessments were applied and blood and urine samples of participants were obtained. Clinical and laboratory assessments were repeated at the 8th week. The last assessments were performed at the 12th week for patients determined as unremitted by clinical assessments. The remission is defined as 17-items Hamilton Depression Scale score of 7 or lower. Liquid chromatography tandem mass spectrometry was used in the measurements of damaged DNA nucleosides in urine samples. The levels of 8-OHdG were adjusted for urine creatinine levels. The levels of OGG1 expressions were determined from cDNA samples, extracted from blood samples, using real time-polymerase chain reaction. Results: Patients with depression have higher levels of 8-OHdG (p=0,008), lower levels of OGG-1 (p=0,024) than healthy controls. Patients with depression presented decreased levels of 8-OHdG (p=0,001), 2,95 fold increased levels of OGG-1 by remission of depressive episode. Conclusion: Our results suggest that patients with depression, compared with healthy volunteers, had more oxidative DNA damage, and that those lesions may be accumulated by reversible impairments of the DNA repair systems. Our data indicate that DNA damage/repair processes are might be involved in neurobiology of depressive episodes. Key words: Depression, DNA damage, DNA repair, 8-OHdG, OGG-1