RESUMEN
Ferroptosis is a new type of iron-dependent cell death caused by lipid peroxide (LPO) accumulation and involved in disease of pulmonary infection. The dysregulation of iron metabolism, the accumulation of LPO, and the inactivation and consumption of glutathione peroxidase 4 (GPX4) are the crucial cause of ferroptosis. Pulmonary infectious diseases caused by Pseudomonas aeruginosa (PA), Mycobacterium tuberculosis (MTB), and severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) are associated with ferroptosis. Ferroptosis may be a potential therapeutic target for pulmonary infectious diseases. However, the mechanisms by which these infections are involved in ferroptosis and whether pulmonary infectious diseases caused by Staphylococcus aureus, Klebsiella pneumoniae, and Leishmania spp are related to ferroptosis are unclear. Accordingly, more researches are needed.Copyright © 2023 Yurong Zhang et al.
RESUMEN
Background: In most serious COVID-19 forms which required prolonged stay in intensive care unit, pulmonary, cardiovascular, renal, neurological and psychological sequelae have been reported after the infection. All these complications can be sustained by chronic inflammatory problems and/ or increased oxidative stress. Material and Methods: Biomarkers of the systemic oxidative stress status (OSS) including enzymatic and non-enzymatic antioxidants, total antioxidant capacity of plasma (PAOT®-Sore), trace elements, oxidative damage to lipids and inflammation markers, were investigated in 12 patients admitted to a revalidation center for post-19 COVID pneumonia. Results: From blood samples collected two months after hospital discharge and one month after admission to the revalidation center, vitamin C, thiol proteins, reduced glutathione, gamma-tocopherol and beta carotene were significantly decreased compared to reference values. By contrast, lipid peroxides and markers of inflammation (neutrophils, myeloperoxidase) were significantly higher than the norms. Lipid peroxides was strongly correlated with Cu (r = 0.95, P < 0.005) and Cu/Zn ratio (0.66, P = 0.020). Using an electrochemical method (PAOT®), total antioxidant capacity (TAC) evaluated in saliva and urine negatively correlated with copper and lipid peroxides. Similar findings were obtained for PAOT®-skin score. Conclusions: Systemic OSS was strongly altered in patients admitted in revalidation after C0VID-19 infection. This suggests the need for supplementing these patients with antioxidants.
RESUMEN
Background: A key role of oxidative stress has been highlighted in the pathogenesis of COVID-19. However, little has been said about oxidative stress status (OSS) of COVID-19 patients hospitalized in intensive care unit (ICU). Material and Methods: Biomarkers of the systemic OSS included antioxidants (9 assays), trace elements (3 assays), inflammation markers (4 assays) and oxidative damage to lipids (3 assays). Results: Blood samples were drawn after 9 (7–11) and 41 (39–43) days of ICU stay, respectively in 3 and 6 patients. Vitamin C, thiol proteins, reduced glutathione, γ-tocopherol, β-carotene and PAOT® score were significantly decreased compared to laboratory reference values. Selenium concentration was at the limit of the lower reference value. By contrast, the copper/zinc ratio (as a source of oxidative stress) was higher than reference values in 55% of patients while copper was significantly correlated with lipid peroxides (r = 0.95, p < 0.001). Inflammatory biomarkers (C-reactive protein and myeloperoxidase) were significantly increased when compared to normals. Conclusions: The systemic OSS was strongly altered in critically ill COVID-19 patients as evidenced by increased lipid peroxidation but also by deficits in some antioxidants (vitamin C, glutathione, thiol proteins) and trace elements (selenium).