Persistent Post COVID-19 Endothelial Dysfunction and Oxidative Stress in Women

Area of Science:

• Biomedical science
• Pathophysiology
• Oxidative stress research

Background:

• Endothelial dysfunction and altered free radical homeostasis are implicated in various pathologies.
• COVID-19 has been associated with significant systemic effects, including potential long-term consequences.

Purpose of the Study:

• To assess endothelial dysfunction and free radical homeostasis in women with and without COVID-19.
• To investigate the impact of acute COVID-19 and asymptomatic infection on oxidative stress markers.
• To evaluate long-term changes in free radical homeostasis 12 months post-COVID-19.

Main Methods:

• Assessed endothelial dysfunction and free radical homeostasis parameters in 92 women (aged 45-69).
• Grouped participants into: control (no COVID-19), acute COVID-19, 12 months post-COVID-19, and asymptomatic COVID-19.
• Measured activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GR), glutathione S-transferases pi (GSTpi), and levels of advanced glycation end products (AGEs), thiobarbituric acid reactants (TBARs), endothelin (END)-1, END-2, 8-OHdG, oxidized glutathione (GSSG), total antioxidant status (TAS), reduced glutathione (GSH), and GSH/GSSG ratio.

Main Results:

• Acute COVID-19 patients showed lower GPx and SOD, decreased AGEs, higher GR, GSTpi, TBARs, END-1, and END-2 compared to controls.
• Asymptomatic COVID-19 group had lower 8-OHdG, GSSG, and TAS, but higher GSH and GSH/GSSG ratio.
• 12 months post-COVID-19, high lipid peroxidation products persisted, indicating long-term free radical imbalance.

Conclusions:

• COVID-19 infection significantly alters endothelial function and free radical homeostasis.
• Persistent oxidative stress and lipid peroxidation post-COVID-19 may contribute to long-term sequelae.
• Understanding these mechanisms is crucial for managing post-COVID conditions.