tetano
Editor, Senior Moderator
Bratisl Lek Listy
. 2022;123(1):9-15.
doi: 10.4149/BLL_2022_002.
Platelet mitochondrial function and endogenous coenzyme Q10 levels are reduced in patients after COVID-19
Z Sumbalova, J Kucharska, P Palacka, Z Rausova, P H Langsjoen, A M Langsjoen, A Gvozdjakova
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).
Keywords: OXPHOS; SARS-CoV-2; coenzyme Q10 oxidative stress.; mitochondria; platelet.
. 2022;123(1):9-15.
doi: 10.4149/BLL_2022_002.
Platelet mitochondrial function and endogenous coenzyme Q10 levels are reduced in patients after COVID-19
Z Sumbalova, J Kucharska, P Palacka, Z Rausova, P H Langsjoen, A M Langsjoen, A Gvozdjakova
- PMID: 34967652
- DOI: 10.4149/BLL_2022_002
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).
Keywords: OXPHOS; SARS-CoV-2; coenzyme Q10 oxidative stress.; mitochondria; platelet.