Glutathione-related antioxidant defence, DNA damage, and DNA repair in patients suffering from post-COVID conditions.

IF 2.5 4区 医学 Q3 GENETICS & HEREDITY Mutagenesis Pub Date : 2023-08-24 DOI:10.1093/mutage/gead021
Selin Kankaya, Fatih Yavuz, Alper Tari, Ahmet Bera Aygun, Esra Gizem Gunes, Bahar Bektan Kanat, Gulru Ulugerger Avci, Hakan Yavuzer, Yildiz Dincer
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Abstract

Post-COVID conditions are defined as the continuation of the symptoms of Coronavirus Disease 2019 (COVID-19) 3 months after the initial Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, with no other explanation. Post-COVID conditions are seen among 30%-60% of patients with asymptomatic or mild forms of COVID-19. The underlying pathophysiological mechanisms of post-COVID conditions are not known. In SARS-CoV-2 infection, activation of the immune system leads to increased production of reactive oxygen molecules, depleted antioxidant reserve, and finally occurrence of oxidative stress. In oxidative stress conditions, DNA damage increases and DNA repair systems impair. In this study, glutathione (GSH) level, glutathione peroxidase (GPx) activity, 8-hydroxydeoxyguanosine (8-OHdG) level, basal, induced, and post-repair DNA damage were investigated in individuals suffering from post-COVID conditions. In the red blood cells, GSH levels and GPx activities were measured with a spectrophotometric assay and a commercial kit. Basal, in vitro H2O2 (hydrogen peroxide)-induced, and post-repair DNA damage (DNA damage after a repair incubation following H2O2-treatment, in vitro) were determined in lymphocytes by the comet assay. The urinary 8-OHdG levels were measured by using a commercial ELISA kit. No significant difference was found between the patient and control groups for GSH level, GPx activity, and basal and H2O2-induced DNA damage. Post-repair DNA damage was found to be higher in the patient group than those in the control group. Urinary 8-OHdG level was lower in the patient group compared to the control group. In the control group, GSH level and post-repair DNA damage were higher in the vaccinated individuals. In conclusion, oxidative stress formed due to the immune response against SARS-COV-2 may impair DNA repair mechanisms. Defective DNA repair may be an underlying pathological mechanism of post-COVID conditions.

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新冠肺炎后患者的谷胱甘肽相关抗氧化防御、DNA损伤和DNA修复。
COVID后情况被定义为首次严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)感染后3个月,2019冠状病毒病(新冠肺炎)症状的持续,没有其他解释。30%至60%的无症状或轻度新冠肺炎患者出现新冠肺炎后症状。新冠肺炎后疾病的潜在病理生理机制尚不清楚。在严重急性呼吸系统综合征冠状病毒2型感染中,免疫系统的激活会导致活性氧分子的产生增加,抗氧化储备耗尽,最终导致氧化应激的发生。在氧化应激条件下,DNA损伤增加,DNA修复系统受损。在本研究中,研究了新冠肺炎后患者的谷胱甘肽(GSH)水平、谷胱甘肽过氧化物酶(GPx)活性、8-羟基脱氧鸟苷(8-OHdG)水平、基础、诱导和修复后DNA损伤。在红细胞中,用分光光度法和商业试剂盒测量GSH水平和GPx活性。通过彗星测定法测定淋巴细胞中的基础、体外H2O2(过氧化氢)诱导的和修复后DNA损伤(体外H2O2处理后修复孵育后的DNA损伤)。通过使用商业ELISA试剂盒测量尿8-OHdG水平。在GSH水平、GPx活性以及基础和H2O2诱导的DNA损伤方面,患者组和对照组之间没有发现显著差异。发现患者组修复后DNA损伤高于对照组。与对照组相比,患者组的尿8-OHdG水平较低。在对照组中,接种疫苗的个体的GSH水平和修复后DNA损伤较高。总之,由针对严重急性呼吸系统综合征冠状病毒2型的免疫反应形成的氧化应激可能损害DNA修复机制。DNA修复缺陷可能是新冠肺炎后疾病的潜在病理机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Mutagenesis
Mutagenesis 生物-毒理学
CiteScore
5.90
自引率
3.70%
发文量
22
审稿时长
6-12 weeks
期刊介绍: Mutagenesis is an international multi-disciplinary journal designed to bring together research aimed at the identification, characterization and elucidation of the mechanisms of action of physical, chemical and biological agents capable of producing genetic change in living organisms and the study of the consequences of such changes.
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