Oxidation of DNA and RNA in young patients with newly diagnosed bipolar disorder and relatives
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Oxidation of DNA and RNA in young patients with newly diagnosed bipolar disorder and relatives. / Coello, Klara; Mäkinen, Ilari Jaakko Olavi; Kjærstad, Hanne Lie; Faurholt-Jepsen, Maria; Miskowiak, Kamilla Woznica; Poulsen, Henrik Enghusen; Vinberg, Maj; Kessing, Lars Vedel.
In: Translational Psychiatry, Vol. 14, No. 1, 81, 2024.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Oxidation of DNA and RNA in young patients with newly diagnosed bipolar disorder and relatives
AU - Coello, Klara
AU - Mäkinen, Ilari Jaakko Olavi
AU - Kjærstad, Hanne Lie
AU - Faurholt-Jepsen, Maria
AU - Miskowiak, Kamilla Woznica
AU - Poulsen, Henrik Enghusen
AU - Vinberg, Maj
AU - Kessing, Lars Vedel
N1 - Publisher Copyright: © The Author(s) 2024.
PY - 2024
Y1 - 2024
N2 - Excessive oxidative stress-generated nucleoside damage seems to play a key role in bipolar disorder (BD) and may present a trait phenomenon associated with familial risk and is one of the putative mechanisms explaining accelerated atherosclerosis and premature cardiovascular diseases (CVD) in younger patients with BD. However, oxidative stress-generated nucleoside damage has not been studied in young BD patients and their unaffected relatives (UR). Therefore, we compared oxidative stress-generated damage to DNA and RNA in young patients newly diagnosed with BD, UR, and healthy control individuals (HC). Systemic oxidative stress-generated DNA and RNA damage levels were compared by analyzing urinary levels of 8-oxo-7,8-dihydro-2′-deoxyguanosine and 8-oxo-7,8-dihydroguanosine in participants aged 15–25 years, including 133 patients newly diagnosed with BD, 57 UR, and 83 HC. Compared with HC, damage to DNA was 21.8% higher in BD patients (B = 1.218, 95% CI = 1.111–1.335, p = <0.001) and 22.5% higher in UR (B = 1.225, 95% CI = 1.090–1.377, p = <0.002), while damage to RNA was 14.8% higher in BD patients (B = 1.148, 95% CI = 1.082–1.219, p = <0.001) and 14.0% higher in UR (B = 1.140, 95% CI = 1.055–1.230, p = < 0.001) in models adjusted for sex and age after correction for multiple comparison. Levels did not differ between patients with BD and UR. Our findings support higher oxidative stress-generated nucleoside damage being a trait phenomenon in BD associated with familial risk and highlight the importance of early diagnosis and treatment to prevent illness progression and development of premature CVD.
AB - Excessive oxidative stress-generated nucleoside damage seems to play a key role in bipolar disorder (BD) and may present a trait phenomenon associated with familial risk and is one of the putative mechanisms explaining accelerated atherosclerosis and premature cardiovascular diseases (CVD) in younger patients with BD. However, oxidative stress-generated nucleoside damage has not been studied in young BD patients and their unaffected relatives (UR). Therefore, we compared oxidative stress-generated damage to DNA and RNA in young patients newly diagnosed with BD, UR, and healthy control individuals (HC). Systemic oxidative stress-generated DNA and RNA damage levels were compared by analyzing urinary levels of 8-oxo-7,8-dihydro-2′-deoxyguanosine and 8-oxo-7,8-dihydroguanosine in participants aged 15–25 years, including 133 patients newly diagnosed with BD, 57 UR, and 83 HC. Compared with HC, damage to DNA was 21.8% higher in BD patients (B = 1.218, 95% CI = 1.111–1.335, p = <0.001) and 22.5% higher in UR (B = 1.225, 95% CI = 1.090–1.377, p = <0.002), while damage to RNA was 14.8% higher in BD patients (B = 1.148, 95% CI = 1.082–1.219, p = <0.001) and 14.0% higher in UR (B = 1.140, 95% CI = 1.055–1.230, p = < 0.001) in models adjusted for sex and age after correction for multiple comparison. Levels did not differ between patients with BD and UR. Our findings support higher oxidative stress-generated nucleoside damage being a trait phenomenon in BD associated with familial risk and highlight the importance of early diagnosis and treatment to prevent illness progression and development of premature CVD.
U2 - 10.1038/s41398-024-02772-8
DO - 10.1038/s41398-024-02772-8
M3 - Journal article
C2 - 38331875
AN - SCOPUS:85184791013
VL - 14
JO - Translational Psychiatry
JF - Translational Psychiatry
SN - 2158-3188
IS - 1
M1 - 81
ER -
ID: 383703032