Evidence map›Paper›PMID 38789433›Full record

ArticleTranslational psychiatry2024

Oxidatively-induced DNA base damage and base excision repair abnormalities in siblings of individuals with bipolar disorder DNA damage and repair in bipolar disorder.

Hidayet Ece Arat Çelik, Selda Yılmaz, İzel Cemre Akşahin, Burcu Kök Kendirlioğlu, Esma Çörekli, Nazlı Ecem Dal Bekar, Ömer Faruk Çelik, Neşe Yorguner, Bilge Targıtay Öztürk, Hüray İşlekel and 4 more

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Article in Translational psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Hidayet Ece Arat ÇelikDepartment of Psychiatry, School of Medicine, Maltepe University, Istanbul, Turkey. ecearat@yahoo.com.ORCID 0000-0002-0880-8974
Selda YılmazDepartment of Molecular Medicine, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.
İzel Cemre AkşahinGraduate School of Health Sciences, Koc University, Istanbul, Turkey.
Burcu Kök KendirlioğluDepartment of Psychiatry, School of Medicine, Maltepe University, Istanbul, Turkey.
Esma ÇörekliDepartment of Psychiatry, School of Medicine, Maltepe University, Istanbul, Turkey.
Nazlı Ecem Dal BekarChair of Proteomics and Bioanalytics, School of Life Sciences, Technical University of Munich, Munich, Germany.
Ömer Faruk ÇelikDepartment of Medical Biochemistry, Sancaktepe Sehit Prof. Dr. Ilhan Varank Training and Research Hospital, Istanbul, Turkey.ORCID 0000-0001-5441-4506
Neşe YorgunerDepartment of Psychiatry, School of Medicine, Marmara University, Istanbul, Turkey.
Bilge Targıtay ÖztürkDepartment of Psychiatry, School of Medicine, Dokuz Eylul University, Izmir, Turkey.ORCID 0000-0002-8524-5204
Hüray İşlekelDepartment of Molecular Medicine, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.
Ayşegül ÖzerdemDepartment of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA.
Pınar AkanDepartment of Neuroscience, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.
Deniz Ceylan *Research Center for Translational Medicine (KUTTAM), School of Medicine, Koc University, Istanbul, Turkey. dozalp@ku.edu.tr.ORCID 0000-0002-1438-8240
Gamze Tuna *Department of Molecular Medicine, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous evidence suggests elevated levels of oxidatively-induced DNA damage, particularly 8-hydroxy-2'-deoxyguanosine (8-OH-dG), and abnormalities in the repair of 8-OH-dG by the base excision repair (BER) in bipolar disorder (BD). However, the genetic disposition of these abnormalities remains unknown. In this study, we aimed to investigate the levels of oxidatively-induced DNA damage and BER mechanisms in individuals with BD and their siblings, as compared to healthy controls (HCs). 46 individuals with BD, 41 siblings of individuals with BD, and 51 HCs were included in the study. Liquid chromatography-tandem mass spectrometry was employed to evaluate the levels of 8-OH-dG in urine, which were then normalized based on urine creatinine levels. The real-time-polymerase chain reaction was used to measure the expression levels of 8-oxoguanine DNA glycosylase 1 (OGG1), apurinic/apyrimidinic endonuclease 1 (APE1), poly ADP-ribose polymerase 1 (PARP1), and DNA polymerase beta (POLβ). The levels of 8-OH-dG were found to be elevated in both individuals with BD and their siblings when compared to the HCs. The OGG1 and APE1 expressions were downregulated, while POLβ expressions were upregulated in both the patient and sibling groups compared to the HCs. Age, smoking status, and the number of depressive episodes had an impact on APE1 expression levels in the patient group while body mass index, smoking status, and past psychiatric history had an impact on 8-OH-dG levels in siblings. Both individuals with BD and unaffected siblings presented similar abnormalities regarding oxidatively-induced DNA damage and BER, suggesting a link between abnormalities in DNA damage/BER mechanisms and familial susceptibility to BD. Our findings suggest that targeting the oxidatively-induced DNA damage and BER pathway could offer promising therapeutic strategies for reducing the risk of age-related diseases and comorbidities in individuals with a genetic predisposition to BD.

Indexed as

8-Hydroxy-2'-DeoxyguanosineBipolar DisorderDNA DamageDNA GlycosylasesDNA RepairOxidative StressSiblingsAdultCase-Control StudiesDeoxyguanosineDNA-(Apurinic or Apyrimidinic Site) LyaseDNA Polymerase betaExcision RepairFemaleHumansMale8-Hydroxy-2'-DeoxyguanosineAPEX1 protein, humanDeoxyguanosineDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesDNA Polymerase betaoxoguanine glycosylase 1, human

Identifiers

PMID38789433
PMCPMC11126633

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.