在COVID-19患者中氧化应激的生物标志物
Elitsa Pavlova1, Petar Atanasov2, Ivaylo Ivanov2
1Faculty of Physics, Sofia University "St. Kliment Ohridski", 1164 Sofia, Bulgaria.
International journal of molecular sciences
|May 7, 2025
概括
COVID-19 感染引发了显著的氧化应激,并抑制了抗氧化剂活性. 这种自由基损伤机制有助于患者的疾病严重性和死亡率.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
背景情况:
- COVID-19与严重的炎症有关.
- 氧化应激是已知的细胞损伤的贡献者.
研究的目的:
- 评估氧化应激作为COVID-19患者细胞损伤的机制.
- 在体内同时评估氧化应激和炎症生物标志物.
主要方法:
- 在COVID-19患者和健康对照中评估血生物标志物.
- 测量了铁酸反应物质 (TBARS),超氧化物脱酶 (SOD),催化酶 (CAT),谷氨酸减少酶 (GRA) 活动和抗氧化能力 (AOC).
- 评估的临床炎症标志物:白细胞 (WBC),淋巴细胞 (LYM),C反应蛋白 (CRP) 和红细胞沉积率 (ESR).
主要成果:
- 在COVID-19患者中,炎症标志物 (WBC,LYM,CRP,ESR) 显著增加.
- 观察到TBARS水平增加 (近3倍) 和SOD活性增加 (近5倍).
- 发现抗氧化能力降低 (超过4倍),GRA活性抑制 (2.5倍),CAT活性增加 (1.4倍).
结论:
- COVID-19 感染与大量的氧化应激和减少的抗氧化剂防御有关.
- 自由基媒介的损害在COVID-19病变发生过程中起着至关重要的作用.
- 这些生化变化可能会导致疾病严重程度,并发症和患者死亡率.
相关概念视频
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