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血小板线粒体功能和内源性辅酶 Q10 水平在 COVID-19 后患者中降低。

Platelet mitochondrial function and endogenous coenzyme Q10 levels are reduced in patients after COVID-19.

出版信息

Bratisl Lek Listy. 2022;123(1):9-15. doi: 10.4149/BLL_2022_002.

DOI:10.4149/BLL_2022_002
PMID:34967652
Abstract

BACKGROUND

After an acute treatment for coronavirus disease (COVID-19), some symptoms may persist for several weeks, for example: fatigue, headaches, muscle and joint pain, cough, loss of taste and smell, sleep and memory disturbances, depression. Many viruses manipulate mitochondrial function, but the exact mechanisms of SARS-CoV-2 virus effect remain unclear. We tested the hypothesis that SARS-CoV-2 virus may affect mitochondrial energy production and endogenous biosynthesis of coenzyme Q10 (CoQ10).

METHODS

Ten patients after COVID-19 and 15 healthy individuals were included in the study. Platelets isolated from peripheral blood were used as an accessible source of mitochondria. High-resolution respirometry for the evaluation of platelets mitochondrial function, and HPLC method for CoQ10 determination were used. Oxidative stress was evaluated by TBARS concentration in plasma.

RESULTS

Platelet mitochondrial respiratory chain function, oxidative phosphorylation and endogenous CoQ10 level were reduced in the patients after COVID-19.

CONCLUSION

We assume that a reduced concentration of endogenous CoQ10 may partially block electron transfer in the respiratory chain resulting in a reduced adenosine triphosphate (ATP) production in the patients after COVID-19. Targeted mitochondrial therapy with CoQ10 supplementation and spa rehabilitation may improve mitochondrial health and accelerate the recovery of the patients after COVID-19. Platelet mitochondrial function and CoQ10 content may be useful mitochondrial health biomarkers after SARS-CoV-2 infection (Tab. 3, Fig. 3, Ref. 46).

摘要

背景

在急性冠状病毒病(COVID-19)治疗后,一些症状可能会持续数周,例如:疲劳、头痛、肌肉和关节疼痛、咳嗽、味觉和嗅觉丧失、睡眠和记忆障碍、抑郁。许多病毒会操纵线粒体功能,但 SARS-CoV-2 病毒的确切作用机制尚不清楚。我们检验了 SARS-CoV-2 病毒可能会影响线粒体能量产生和辅酶 Q10(CoQ10)内源性生物合成的假设。

方法

本研究纳入了 10 名 COVID-19 后患者和 15 名健康个体。从外周血中分离的血小板被用作线粒体的可及来源。使用高分辨率呼吸测定法评估血小板线粒体功能,使用 HPLC 法测定 CoQ10 水平。通过血浆中 TBARS 浓度评估氧化应激。

结果

COVID-19 后患者的血小板线粒体呼吸链功能、氧化磷酸化和内源性 CoQ10 水平降低。

结论

我们假设内源性 CoQ10 浓度降低可能会部分阻断呼吸链中的电子转移,从而导致 COVID-19 后患者的三磷酸腺苷(ATP)生成减少。用 CoQ10 补充和水疗康复进行靶向线粒体治疗可能会改善线粒体健康并加速 COVID-19 后患者的康复。血小板线粒体功能和 CoQ10 含量可能是 SARS-CoV-2 感染后有用的线粒体健康生物标志物(表 3,图 3,参考文献 46)。

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