Alteration of circulating redox balance in coronavirus disease-19-induced acute respiratory distress syndrome

Francesco Bellanti; Sławomir Kasperczyk; Aleksandra Kasperczyk; Michał Dobrakowski; Gabriella Pacilli; Giuseppina Vurchio; Alessandro Maddalena; Stefano Quiete; Aurelio Lo Buglio; Cristiano Capurso; Gaetano Serviddio; Gianluigi Vendemiale

doi:10.1186/s40560-023-00679-y

Alteration of circulating redox balance in coronavirus disease-19-induced acute respiratory distress syndrome

J Intensive Care. 2023 Jul 5;11(1):30. doi: 10.1186/s40560-023-00679-y.

Affiliations

¹ Department of Medical and Surgical Sciences, University of Foggia, Viale Pinto, 1, 71122, Foggia, Italy. francesco.bellanti@unifg.it.
² Department of Biochemistry, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, 41-808, Zabrze, Poland.
³ Department of Medical and Surgical Sciences, University of Foggia, Viale Pinto, 1, 71122, Foggia, Italy.

Abstract

Background: Mechanisms underpinning ARDS induced by COVID-19 are mostly immune-mediated, but need to be completely clarified. This study aimed to investigate redox balance in COVID-19 patients with ARDS, trying to recognize possible differences from typical ARDS related to the pathophysiology of severe disease.

Methods: Patients affected by ARDS and positive for the SARS-CoV-2 virus (N = 40, COVID-19) were compared to ARDS patients negative to the molecular test (N = 42, No COVID-19). Circulating markers of redox balance were measured in serum and erythrocytes, and related to markers of inflammation and coagulability.

Results: No differences in serum markers of oxidative damage were found between both groups, but a reduction in total antioxidant status and serum ceruloplasmin level was observed in COVID-19 rather than No COVID-19 patients. Redox balance alterations were described in erythrocytes from COVID-19 with respect to No COVID-19 group, characterized by increased lipofuscin and malondialdehyde concentration, and reduced glutathione S-transferase and glutathione reductase activity. These markers were associated with circulating indexes of respiratory disease severity (Horowitz index and alveolar-to-arterial oxygen gradient), inflammation (interleukin-6 and interleukin-10), and hypercoagulability (D-dimer) in COVID-19 patients with ARDS.

Conclusions: ARDS caused by COVID-19 is sustained by impairment of redox balance, particularly in erythrocytes. This alteration is associated with the pro-inflammatory and pro-coagulant status which characterizes severe COVID-19.

Keywords: Acute respiratory distress syndrome; COVID-19; Erythrocyte oxidative stress; Hypercoagulability; Inflammation; Redox-dependent markers; Respiratory failure.