Increased serum levels of 8-hydroxy-2'-deoxyguanosine in clinical depression

• Published in: Psychosomatic medicine Vol. 68; no. 1; pp. 1 - 7
• Main Authors: Forlenza, Michael J, Miller, Gregory E
• Format: Journal Article
• Language: English
• Published: United States Lippincott Williams & Wilkins Ovid Technologies 01-01-2006
• Subjects: Adult; Biomarkers - blood; Deoxyguanosine - analogs & derivatives; Deoxyguanosine - blood; Depressive Disorder - blood; Depressive Disorder - physiopathology; DNA damage; DNA Damage - physiology; Female; Humans; Male; Mental depression; Oxidation; Oxidative Stress - physiology
• ISSN: 0033-3174; 1534-7796
• DOI: 10.1097/01.psy.0000195780.37277.2a

We sought to understand the pathophysiological effects of depression by examining group differences in serum levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of oxidative damage.
Our sample consisted of 169 participants. Eight-four of these participants met diagnostic criteria for clinical depression. The 85 participants in our comparison group were matched on age, gender, and ethnicity to the depressed group. 8-OHdG was measured by enzyme-linked immunosorbent assay.
After adjusting for age, gender, race/ethnicity, years of education, daily smoking, average number of alcoholic drinks per week, average amount of physical activity per week, and body mass index, participants in the depressed group had significantly higher levels of oxidative DNA damage compared with participants in the control group. Pairwise comparisons showed that participants with major depression had significantly higher levels of 8-OHdG than control subjects and marginally higher levels of 8-OHdG compared with those with minor depression. Furthermore, participants with recurrent episodes of depression had more oxidative damage than participants with single episodes, who in turn had more damage than healthy control subjects. Finally, participants with recurrent episodes of major depression had more DNA damage than other depressed participants, who in turn had more damage than healthy control subjects.
Our findings suggest that increased oxidative damage may represent a common pathophysiological mechanism, whereby depressed individuals become vulnerable to comorbid medical illness.