Purpose: The measurement of biomarkers in exhaled breath condensate (EBC) offers a non-invasive way to assess airway disease and can be easily done in a clinical setting among patients with cystic fibrosis (CF). The role of oxidative and nitrosative stress in the complex pathophysiology of CF is widely accepted and biomarkers of oxidative and nitrosative stress can be measured in the serum and EBC. To our knowledge, this is the first study to assess markers of nitrosative stress in EBC and serum, collected simultaneously from the CF patients.
Patients And Methods: Paired EBC and serum samples were collected from 36 stable patients with CF and 14 healthy controls. Markers of nitrosative stress ‒ 3-nitrotyrosine and nitrate/nitrite were measured in the EBC and serum using an enzyme-linked immunosorbent assay.
Results: We found no differences in 3-nitrotyrosine and nitrate/nitrite in the EBC of patients with CF as compared to healthy controls (125.37 ± 3.29 vs. 126.24 ± 2.21 nmol/L, p = 0.218; 12.66 ± 7.23 vs. 8.79 ± 4.83 μmol/L, p = 0.133, respectively). Furthermore, 3-nitrotyrosine and nitrate/nitrite were significantly higher in the serum of patients with CF as compared to the healthy controls (0.13 ± 0.02 vs. 0.11 ± 0.01 nmol/mg protein, p = 0.003; 70.78 ± 22.55 vs. 53.08 ± 8.5 μmol/L, p = 0.009, respectively). No correlations were found between the markers determined in the EBC and serum.
Conclusions: The results of the EBC nitrosative stress biomarkers should be interpreted with caution, especially in patients with stable disease, as the EBC values may be independent on levels of circulating markers that are elevated in the serum of patients with stable CF.
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http://dx.doi.org/10.1016/j.advms.2023.05.002 | DOI Listing |
Metabol Open
March 2025
Hepatogastroenterology and Infectious Diseases Department, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
Background: Tissue damage by viral hepatitis is a major cause of morbidity and mortality worldwide. Oxidation reactions and reactive oxygen species (ROS) transform proteins and lipids in plasma low-density lipoproteins (LDL) into the abnormal oxidized LDL (ox-LDL). Hepatitis C virus (HCV) infection induces oxidative/nitrosative stress from multiple sources, including the inducible nitric oxide synthase (iNOS), the mitochondrial electron transport chain, hepatocyte NAD(P)H oxidases (NOX enzymes), and inflammation.
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January 2025
Laboratory of Molecular Biology and Immunology, Department of Pharmacy, University of Patras, 26500, Rio-Patras, Greece.
Taurine, although not a coding amino acid, is the most common free amino acid in the body. Taurine has multiple and complex functions in protecting mitochondria against oxidative-nitrosative stress. In this comprehensive review paper, we introduce a novel potential role for taurine in protecting from deuterium (heavy hydrogen) toxicity.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Biological Sciences, University of Calgary, Calgary, AB, T2N 1N4, Canada.
Metals have been used throughout history to manage disease. With the rising incidence of antibiotic-resistant bacterial strains, metal-based antimicrobials (MBAs) have re-emerged as an alternative to combat infections. Gallium nitrate has shown promising efficacy against several pathogens.
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January 2025
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Autophagy is a protective mechanism of cardiomyocytes. Hyperhomocysteinemia (HHcy) elevates oxidative and nitrosative stress levels, leading to an abnormal increase in nitration protein, possibly leading to abnormal autophagy regulation in cardiomyocytes. However, the regulatory effect of HHcy on autophagy at the post-translational modification level is still unclear.
View Article and Find Full Text PDFPharmaceutics
November 2024
Laboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea.
Ischemic stroke (IS) remains a leading cause of mortality and long-term disability worldwide, with limited therapeutic options available. Despite the success of early interventions, such as tissue-type plasminogen activator administration and mechanical thrombectomy, many patients continue to experience persistent neurological deficits. The pathophysiology of IS is multifaceted, encompassing excitotoxicity, oxidative and nitrosative stress, inflammation, and blood-brain barrier disruption, all of which contribute to neural cell death, further complicating the treatment of IS.
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