The classical nicotinamide adenine dinucleotide phosphate (NADPH) oxidase was originally detected in neutrophils as a multicomponent enzyme that catalyzes the generation of superoxide from oxygen and the reduced form of NADPH. This enzyme is composed of two membrane-bound subunits (p22phox and gp91phox), three cytosolic subunits (p67phox, p47phox, and p40phox) and a small G-protein Rac (Rac1 and Rac2). Recently, it has been demonstrated that there are several isoforms of nonphagocytic NADPH oxidase. Endothelial cells, vascular smooth muscle cells or adventitial fibroblasts possess multiple isoforms of this enzyme. The new homologs, along with gp91phox are now designated the Nox family of NADPH oxidases and are key sources of reactive oxygen species in the vasculature. Reactive oxygen species play a significant role in regulating endothelial function and vascular tone. However, besides the participation in the processes of physiological cell, these enzymes can also be the perpetrator of oxidative stress that causes endothelial dysfunction. This review summarizes the current state of knowledge of the structure and functions of NADPH oxidase and NADPH oxidase inhibitors in the treatment of disorders with endothelial damage.

The COVID‐19 pandemic caused relatively high mortality in patients, especially in those with concomitant diseases (i.e., diabetes, hypertension, and chronic obstructive pulmonary disease (COPD)). In most of aforementioned comorbidities, the oxidative stress appears to be an important player in their pathogenesis. The direct cause of death in critically ill patients with COVID‐19 is still far from being elucidated. Although some preliminary data suggests that the lung vasculature injury and the loss of the functioning part of pulmonary alveolar population are crucial, the precise mechanism is still unclear. On the other hand, at least two classes of medications used with some clinical benefits in COVID‐19 treatment seem to have a major influence on ROS (reactive oxygen species) and RNS (reactive nitrogen species) production. However, oxidative stress is one of the important mechanisms in the antiviral immune response and innate immunity. Therefore, it would be of interest to summarize the data regarding the oxidative stress in severe COVID‐19. In this review, we discuss the role of oxidative and antioxidant mechanisms in severe COVID‐19 based on available studies. We also present the role of ROS and RNS in other viral infections in humans and in animal models. Although reactive oxygen and nitrogen species play an important role in the innate antiviral immune response, in some situations, they might have a deleterious effect, e.g., in some coronaviral infections. The understanding of the redox mechanisms in severe COVID‐19 disease may have an impact on its treatment.

The aim of the present study was to assess synbiotic (Lactobacillus casei + inulin) influence on oxidative stress parameters such as concentrations of malondialdehyde (MDA), hydrogen peroxide (H₂O₂), glutathione, and free sulfhydryl groups content. Experiments were carried out on healthy volunteers (n = 32). The subjects were divided into women group (n = 16) and men group (n = 16) and randomly assigned to synbiotic and control groups. Blood samples were collected before synbiotic supplementation and after 7 wks, at the end of the study. The administration of synbiotic resulted in a significant decrease in MDA (p < 0.01), H₂O₂ (p < 0.01), and GSSG concentrations (p < 0.05) as compared with the control groups and significant increase in the concentrations of GSHt (p < 0.001), GSH (p < 0.01), and ‐SH group content (p < 0.05) versus control. Synbiotics containing L. casei plus inulin may have positive influence on selected oxidative stress markers.

The aim of the present study was to assess whether BAY 11-7082, a nuclear factor-kappaB (NF-κB) inhibitor, influences the level of reactive oxygen species (ROS), tumor necrosis factor alpha (TNF-α), and NF-κB related signaling pathways in the liver. The animals were divided into 4 groups: I: saline; II: saline + endothelin-1 (ET-1) (1.25 μg/kg b.w., i.v.); III: saline + ET-1 (12.5 μg/kg b.w., i.v.); and IV: BAY 11-7082 (10 mg/kg b.w., i.v.) + ET-1 (12.5 μg/kg b.w., i.v.). Injection of ET-1 alone at a dose of 12.5 μg/kg b.w. showed a significant (P<0.001) increase in thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (H₂O₂) level and decrease (P<0.01) in GSH level (vs. control). ET-1 administration slightly downregulated gene expression of p65 of NF-κB but potently and in a dose-dependent way downregulated p21-cip gene expression in the liver. BAY 11-7082 significantly decreased TBARS (P<0.001), H₂O₂(P<0.01) and improved the redox status (P<0.05), compared to ET-1 group. The concentration of TNF-αwas increased in the presence of ET-1 (P<0.05), while BAY 11-7082 decreased TNF-αconcentration (P<0.01). Inhibition of IkBαbefore ET-1 administration downregulated gene expression of p21-cip but had no effect on p65.

Background: Asthma (a chronic inflammatory disease of the airways) is characterized by a variable course, response to treatment, and prognosis. Its incidence has increased significantly in recent decades. Unfortunately, modern lifestyle and environmental factors contribute to the further increase in the incidence of this disease. Progressive industrialization and urbanization, widespread use of antibiotic therapy, excessive sterility and inappropriate, highly processed diets are some of the many risk factors that are relevant today. Over the years, a lot of evidence has been gathered showing the influence of microorganisms of the gut or airways on human health. Studies published in recent years indicate that dysbiosis (microbial imbalance) and oxidative stress (pro-oxidant–antioxidant imbalance) are important elements of the pathogenesis of this inflammatory disease. Scientists have attempted to counteract the effects of this process by using probiotics, prebiotics, and antioxidants. The use of probiotic microorganisms positively modulates the immune system by maintaining homeostasis between individual fractions of immune system cells. Moreover, recently conducted experiments have shown that probiotics have antioxidant, anti-inflammatory, and protective properties in oxidative stress (OS). The aim of this study is to present the current state of knowledge on the role of dysbiosis and OS in the pathogenesis of asthma. Conclusions: This review highlights the importance of using probiotics, prebiotics, and antioxidants as potential strategies to support the treatment and prevention of this disease.