Role of oxidative stress in the severity of SARS-COV-2 infection

Since the World Health Organization declared SARS-CoV-2 (COVID-19) a pandemic in March 2020, serious efforts have been made to understand the epidemiology, molecular mechanisms, pathology, and clinical evolution of this disease. Oxidative stress (OX-S) has been implicated in the etiologies of many diseases, including SARS-CoV-2. Recent studies suggest that superoxide radicals and the products of lipid peroxidation, such as the electrophilic aldehyde, 4-hydroxynonenal (4-HNE), are important mediators of the pathological effects of oxidative stress during microbial and viral infections. Numerous studies have confirmed that viral infections induce inflammatory responses that generate excessive amounts of reactive oxygen species and 4-HNE protein adducts in plasma and in various tissues, including alveolar epithelium and endothelium. In this book chapter, we will highlight and discuss the apparent and plausible relationships between SARS-CoV-2 virulence and oxidative stress/lipid peroxidation, which affect cellular and DNA repair mechanisms and immune response. © 2023 Elsevier Inc. All rights reserved.

Selenium Status and Oxidative Stress in SARS-CoV-2 Patients.

Background and Objectives: Insufficient intake of essential micronutrient selenium (Se) increases the susceptibility to diseases associated with oxidative stress. The study aim was to assess Se status and oxidative stress in COVID-19 patients depending on severity of the disease. Materials and Methods: Blood plasma of 80 post-COVID-19 disease patients and 40 acutely ill patients were investigated. Concentration of Se was detected by a fluorometric method with di-amino-naphthalene using acidic hydrolysis. Selenoprotein P (Sepp1), malondialdehyde (MDA), and 4-hydroxynonenal (4-HNE) and their metabolite adducts were evaluated by spectrophotometric methods using commercial assay kits. Results: Obtained results demonstrated that Se and Sepp1 concentration in acute patients were significantly (p < 0.05 for Se and p < 0.001 for Sepp1) decreased compared with post-COVID-19 disease patients. However, in post-COVID-19 disease patients, Se values were close to the low limit of the norm for the European population. 4-HNE adducts concentration as a marker of lipid peroxidation was significantly increased in the acute patients group compared to the recovery group (p < 0.001). Conclusions: COVID-19 pathology is characterized by the induction of oxidative stress and suppression of antioxidant defenses during the acute phase. Lower levels of Se and Sepp1 and higher levels of reactive oxygen species reflect this imbalance, highlighting the role of oxidative stress in the disease's pathogenesis.

The Impact of Severe COVID-19 on Plasma Antioxidants.

Several studies suggested the association of COVID-19 with systemic oxidative stress, in particular with lipid peroxidation and vascular stress. Therefore, this study aimed to evaluate the antioxidant signaling in the plasma of eighty-eight patients upon admission to the Clinical Hospital Dubrava in Zagreb, of which twenty-two died within a week, while the other recovered. The differences between the deceased and the survivors were found, especially in the reduction of superoxide dismutases (SOD-1 and SOD-2) activity, which was accompanied by the alteration in glutathione-dependent system and the intensification of the thioredoxin-dependent system. Reduced levels of non-enzymatic antioxidants, especially tocopherol, were also observed, which correlated with enhanced lipid peroxidation (determined by 4-hydroxynonenal (4-HNE) and neuroprostane levels) and oxidative modifications of proteins assessed as 4-HNE-protein adducts and carbonyl groups. These findings confirm the onset of systemic oxidative stress in patients with severe SARS-CoV-2, especially those who died from COVID-19, as manifested by strongly reduced tocopherol level and SOD activity associated with lipid peroxidation. Therefore, we propose that preventive and/or supplementary use of antioxidants, especially of lipophilic nature, could be beneficial for the treatment of COVID-19 patients.

Gastrointestinal tissue as a "new" target of pollution exposure.

Airborne pollution has become a leading cause of global death in industrialized cities and the exposure to environmental pollutants has been demonstrated to have adverse effects on human health. Among the pollutants, particulate matter (PM) is one of the most toxic and although its exposure has been more commonly correlated with respiratory diseases, gastrointestinal (GI) complications have also been reported as a consequence to PM exposure. Due to its composition, PM is able to exert on intestinal mucosa both direct damaging effects, (by reaching it either via direct ingestion of contaminated food and water or indirect inhalation and consequent macrophagic mucociliary clearance) and indirect ones via generation of systemic inflammation. The relationship between respiratory and GI conditions is well described by the lung-gut axis and more recently, has become even clearer during coronavirus disease 2019 (COVID-19) pandemic, when respiratory symptoms were associated with gastrointestinal conditions. This review aims at pointing out the mechanisms and the models used to evaluate PM induced GI tract damage.