AbstractPrevious 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.

摘要先前的证据表明，氧化诱导的DNA损伤水平升高，特别是8-羟基-2'-脱氧鸟苷（8-OH-dG），以及双相情感障碍（BD）中碱基切除修复（BER）修复8-OH-dG的异常。但是，这些异常的遗传处置仍然未知。

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.

在这项研究中，我们旨在调查与健康对照（HC）相比，BD患者及其兄弟姐妹的氧化诱导DNA损伤水平和BER机制。该研究包括46名BD患者，41名BD患者的兄弟姐妹和51名HC。液相色谱-串联质谱法用于评估尿液中8-OH-dG的水平，然后根据尿肌酐水平对其进行标准化。

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.

实时聚合酶链反应用于测量8-氧鸟嘌呤DNA糖基化酶1（OGG1），嘌呤/嘧啶核酸内切酶1（APE1），聚ADP核糖聚合酶1（PARP1）和DNA聚合酶β（POLβ）的表达水平。与HC相比，BD患者及其兄弟姐妹的8-OH-dG水平均升高。

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.

与HC相比，患者和兄弟姐妹组的OGG1和APE1表达均下调，而POLβ表达均上调。年龄，吸烟状况和抑郁发作次数对患者组的APE1表达水平有影响，而体重指数，吸烟状况和既往精神病史对兄弟姐妹的8-OH-dG水平有影响。

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.

患有BD和未受影响兄弟姐妹的个体在氧化诱导的DNA损伤和BER方面均表现出类似的异常，这表明DNA损伤/BER机制异常与BD的家族易感性之间存在联系。我们的发现表明，针对氧化诱导的异常。

IntroductionBipolar disorder (BD) is a chronic mood disorder that often co-occurs with various medical illnesses and is associated with premature aging, resulting in a shortened life expectancy [1]. Mounting evidence suggests that individuals with BD have elevated levels of oxidatively-induced DNA damage [2,3,4].

引言双相情感障碍（BD）是一种慢性情绪障碍，常与各种医学疾病同时发生，并与过早衰老有关，导致预期寿命缩短。越来越多的证据表明，BD患者的氧化诱导DNA损伤水平升高[2，3，4]。

DNA is a highly susceptible molecule to oxidative insults, and it is estimated that every single cell of the human body is exposed to up to a million DNA lesions [5, 6]. Nevertheless, these damages are repaired by the cellular DNA repair machinery, which includes the base excision repair (BER). However, an overload of oxidative insults or insufficient repair can lead to persistent DNA damage, genomic instability, and ultimately, premature aging and the development of various illnesses [6].

DNA是一种高度易受氧化损伤的分子，据估计，人体的每个细胞都会暴露于多达一百万个DNA损伤[5，6]。然而，这些损伤是由细胞DNA修复机制修复的，其中包括碱基切除修复（BER）。然而，过多的氧化损伤或修复不足会导致持续的DNA损伤，基因组不稳定，最终导致过早衰老和各种疾病的发展。

Therefore, oxidatively-induced DNA damage and abnormal DNA repair mechanisms have been suggested to play a crucial role in the shared pathophysiology among BD, increased cellular aging, and comorbidity [7,8,9,10].The 8-hydroxy-2’-deoxyguanosine (8-OH-dG) is formed by the attack of the hydroxyl radical at the C8-position of guanine of dG followed by the one-electron oxidation of the OH-adduct radical of guanine [11, 12].

因此，氧化诱导的DNA损伤和异常的DNA修复机制已被认为在BD之间共享的病理生理学，增加的细胞衰老和合并症中起着至关重要的作用[7,8,9,10]。8-羟基-2'-脱氧鸟苷（8-OH-dG）是由dG鸟嘌呤C8位的羟基自由基攻击，然后鸟嘌呤的OH加合自由基单电子氧化而形成的[11，12]。

Since guanine is the most susceptible base to oxidation due to its low reduction potential, 8-OH-dG is the most widely used parameter to determine oxidatively-induced DNA damage [13, 14]. Alongside 8-hydroxyguanine (8-OH-Gua), various purine and pyrimidine base damages such as 8-hydroxyadenine (8-OH-Ade), 4,6-diamino-5-formamidopyrimidine (FapyAde), 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua), cytosine glycol (Cyt gly), thymine glycol (Thy gly), 5-hydroxymethyluracil (5-OH-MeUra), and 5,6-dihydroxycytosine exist.

由于鸟嘌呤由于其低还原电位而最容易被氧化，因此8-OH-dG是确定氧化诱导的DNA损伤的最广泛使用的参数[13，14]。除了8-羟基鸟嘌呤（8-OH-Gua）之外，还存在各种嘌呤和嘧啶碱损伤，例如8-羟基腺嘌呤（8-OH-Ade），4,6-二氨基-5-甲酰胺嘧啶（FapyAde），2,6-二氨基-4-羟基-5-甲酰胺嘧啶（FapyGua），胞嘧啶乙二醇（Cyt-gly），胸腺嘧啶乙二醇（Thy-gly），5-羟甲基尿嘧啶（5-OH-MeUra）和5,6-二羟基胞嘧啶。

In contrast to the numerous well-esta.

与众多的esta油井形成对比。

Data availability

数据可用性

All data will be made available upon request.

所有数据将根据要求提供。

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Download referencesAcknowledgementsThis research was funded by the Dokuz Eylul University Scientific Research Project Scholarship and Lithium Association Scholarship. In addition, this project was awarded an encouragement prize by the Psychiatric Association of Turkey. The authors gratefully acknowledge the use of the services and facilities of the Koç University Research Center for Translational Medicine (KUTTAM), funded by the Presidency of Turkey, Head of Strategy and Budget.

下载参考文献致谢本研究由Dokuz Eylul大学科学研究项目奖学金和锂协会奖学金资助。此外，该项目还获得了土耳其精神病学协会颁发的鼓励奖。作者非常感谢使用科萨大学转化医学研究中心（KUTTAM）的服务和设施，该中心由土耳其总统兼战略和预算负责人资助。

Koç University funded the publication.Author informationAuthor notesThese authors contributed equally: Deniz Ceylan, Gamze Tuna.Authors and AffiliationsDepartment of Psychiatry, School of Medicine, Maltepe University, Istanbul, TurkeyHidayet Ece Arat Çelik, Burcu Kök Kendirlioğlu & Esma ÇörekliDepartment of Molecular Medicine, Institute of Health Sciences, Dokuz Eylul University, Izmir, TurkeySelda Yılmaz, Hüray İşlekel & Gamze TunaGraduate School of Health Sciences, Koc University, Istanbul, Turkeyİzel Cemre AkşahinResearch Center for Translational Medicine (KUTTAM), School of Medicine, Koc University, Istanbul, Turkeyİzel Cemre Akşahin & Deniz CeylanChair of Proteomics and Bioanalytics, School of Life Sciences, Technical University of Munich, Munich, GermanyNazlı Ecem Dal BekarDepartment of Medical Biochemistry, Sancaktepe Sehit Prof.

科萨大学资助了该出版物。作者信息作者注意到这些作者做出了同样的贡献：Deniz Ceylan，Gamze Tuna。作者和附属机构伊斯坦布尔马尔特佩大学医学院精神病学系，土耳其希达耶Ece AratÇelik，Burcu KöK Kendirlioğlu＆EsmaÇrekliDepartment of Molecular Medicine，Institute of Health Sciences，Dokuz Eylul大学，伊兹密尔，土耳其塞尔达Yılmaz，Hürayİşlekel＆Gamze Tunahin Koc大学健康科学研究生院，土耳其伊斯坦布尔İzel Cemre AkşahinResearch Center for Translational Medicine（KUTTAM），土耳其伊斯坦布尔Koc大学医学院İzel Cemre Akşahin＆Deniz CeylanChair of Proteomics and Bioanalytics，School of Life Sciences，Technical University of Munich，Munich，GermanyNazlıEcem Dal Bekard医学生物化学系，Sancaktepe Sehit教授。

Dr. Ilhan Varank Training and Research Hospital, Istanbul, TurkeyÖmer Faruk ÇelikDepartment of Psychiatry, School of Medicine, Marmara University, Istanbul, TurkeyNeşe YorgunerDepartment of Psychiatry, School of Medicine, Dokuz Eylul University, Izmir, TurkeyBilge Targıtay ÖztürkDepartment of Medical Biochemistry, School of Medicine, Dokuz Eylul University, Izmir, TurkeyHüray İşlekelDepartment of Psychiatry and Psychology, Mayo Clinic, Rochester, .

Ilhan Varank医生培训和研究医院，土耳其伊斯坦布尔Ömer FarukÇelik马尔马拉大学医学院精神病学系，伊斯坦布尔，土耳其Neşe Yorguer医学院，伊兹密尔，土耳其Bilge TargıtayÖztürkDokuz Eylul大学医学院医学生物化学系，伊兹米尔，土耳其Hüray Work lekel梅奥诊所精神病学和心理学系。

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PubMed Google ScholarContributionsInterviews with the participants were conducted by HEAÇ, BKK, EÇ, NY, and BTÖ. The laboratory analyses were conducted by HEAÇ, SY, İCA, NEDB, ÖFÇ, Hİ, PA, DC, and GT. Statistical analyses were performed by HEAÇ and DC. The conceptualization of the study was undertaken by HEAÇ, AÖ, PA, DC, and GT.

PubMed谷歌学术贡献与参与者的互动新闻由HEAÇ，BKK，EÇ，NY和BTÖ进行。实验室分析由HEAÇ，SY，İCA，NEDB，ÖFÇ，Hİ，PA，DC和GT进行。统计分析由HEAÇ和DC进行。该研究的概念化由HEAÇ，AÖ，PA，DC和GT进行。

The manuscript was revised by HEAÇ, SY, İCA, BKK, EÇ, NEDB, ÖFÇ, NY, BTÖ, Hİ, AÖ, PA, DC, and GT.Corresponding authorsCorrespondence to.

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Reprints and permissionsAbout this articleCite this articleArat Çelik, H.E., Yılmaz, S., Akşahin, İ.C. et al. Oxidatively-induced DNA base damage and base excision repair abnormalities in siblings of individuals with bipolar disorder DNA damage and repair in bipolar disorder.

转载和许可本文引用本文AratÇelik，H.E.，Yılmaz，S.，Akşahin，İ。C、 双相情感障碍患者兄弟姐妹中氧化诱导的DNA碱基损伤和碱基切除修复异常双相情感障碍中的DNA损伤和修复。

Transl Psychiatry 14, 207 (2024). https://doi.org/10.1038/s41398-024-02901-3Download citationReceived: 17 August 2023Revised: 01 April 2024Accepted: 05 April 2024Published: 24 May 2024DOI: https://doi.org/10.1038/s41398-024-02901-3Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard.

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