Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Mutagenesis. 2023 Aug 24;38(4):216-226. doi: 10.1093/mutage/gead021.
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.
新冠后(post-COVID)状况被定义为在初次感染严重急性呼吸综合征冠状病毒 2 型（SARS-CoV-2）后 3 个月仍持续存在新冠病毒疾病 2019（COVID-19）症状，且无其他解释。新冠后(post-COVID)状况可见于无症状或轻症 COVID-19 患者的 30%-60%。新冠后(post-COVID)状况的潜在病理生理机制尚不清楚。在 SARS-CoV-2 感染中，免疫系统的激活导致活性氧分子的产生增加，抗氧化储备耗尽，最终发生氧化应激。在氧化应激条件下，DNA 损伤增加，DNA 修复系统受损。在这项研究中，我们研究了患有新冠后(post-COVID)状况的个体的谷胱甘肽（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。用分光光度法和商业试剂盒测量红细胞中的 GSH 水平和 GPx 活性。通过彗星试验在淋巴细胞中测定基础、体外 H2O2（过氧化氢）诱导和修复后 DNA 损伤（H2O2 处理后修复孵育后的 DNA 损伤，体外）。使用商业 ELISA 试剂盒测量尿 8-OHdG 水平。患者组和对照组之间的 GSH 水平、GPx 活性以及基础和 H2O2 诱导的 DNA 损伤没有显著差异。与对照组相比，患者组的修复后 DNA 损伤更高。与对照组相比，患者组的尿 8-OHdG 水平较低。在对照组中，接种个体的 GSH 水平和修复后 DNA 损伤更高。总之，针对 SARS-COV-2 的免疫反应产生的氧化应激可能会损害 DNA 修复机制。有缺陷的 DNA 修复可能是新冠后(post-COVID)状况的潜在病理机制。
