Association Between Plasma Redox State/Mitochondria Function and a Flu-Like Syndrome/COVID-19 in the Elderly Admitted to a Long-Term Care Unit

Abstract

Background/Aims: It is widely known that the imbalance between reactive oxygen species (ROS)/antioxidants and mitochondrial function could play a pivotal role in aging and in the physiopathology of viral infections. Here, we correlated the plasma oxidants/antioxidants levels of the elderly admitted to a long-term care (LTC) unit with clinical data in relation to flu-like disease/COVID-19. Moreover, in vitro we examined the effects of plasma on cell viability, ROS release and mitochondrial function.Materials and Methods: In 60 patients admitted to LTC unit for at least 1 year at moderate or high care load, demographic and clinical variables were taken. Blood samples were collected for the evaluations of oxidants/antioxidants, as thiobarbituric acid reactive substances, 8-hydroxy-2-deoxyguanosine, 8-isoprostanes, superoxide dismutase activity, glutathione, and vitamin D. In vitro, human umbilical vascular endothelial cells (HUVEC) were used to examine the effects of plasma on viability, ROS release and mitochondrial membrane potential.Results: The results obtained showed that the redox state of the elderly was quite balanced; mitochondrial membrane potential of HUVEC was reduced by about 20%, only. Also, the correlation analysis evidenced the association between mitochondrial function and the patients’ outcomes. Interestingly, lower levels of mitochondrial membrane potential were found in the elderly who had symptoms suggestive of COVID-19 or with a confirmed diagnosis of COVID-19.Conclusion: The results of this study highlight the importance of mitochondrial function in the tendency to get a flu-like syndrome like COVID-19 in the elderly admitted to LTC unit. This information could have clinical implications for the management of old population.

The SARS-CoV-2 Spike protein induces long-term transcriptional perturbations of mitochondrial metabolic genes, causes cardiac fibrosis, and reduces myocardial contractile in obese mice

“…For example, evidence has shown mitochondrial dysfunction, metabolic alterations with an increase in glycolysis, and high levels of mitokine in PBMCs from patients with COVID-19 [40]. Lower levels of mitochondrial membrane potential were found in the elderly who had symptoms suggestive of COVID-19 or with a confirmed diagnosis of COVID-19 [41]. SARS-CoV-2 can cause transcriptional downregulation of mitochondria-related processes, respiratory electron transport chain, and ATP synthesis coupled electron transport in the lung epithelial cell line A549 [42].…”

DNA damage and inflammation in COVID-19 cases

“…Increasing ROS has the capacity to change macromolecules over time. The resulting macromolecular damage contributes to many mechanisms underlying the progression of COVID-19 disease 16 . Therefore, biomarkers of DNA damage are extremely important.…”

Understanding Long COVID; Mitochondrial Health and Adaptation—Old Pathways, New Problems

“…It has also been found that in the leukocytes of patients with post COVID-19 sequalae there is evidence of decreased mitochondrial membrane potential [ 73 ], while in an elderly population, a decreased mitochondrial membrane potential seemed to associate with an increased susceptibility and vulnerability to the virus [ 74 ]. Another observation is that in placental samples from infected patients, SARS-CoV-2 RNA co-localised with mitochondria, which was associated with altered mitochondrial networks [ 75 ] and although one study did not find any changes in mitochondrial long non-coding RNAs during infection, during recovery, there was a persistence change in small mitochondrial RNAs [ 76 ].…”