Oxidative stress and inflammation biomarkers in pulmonary tuberculosis
Journal Title: Moldovan Medical Journal - Year 2017, Vol 60, Issue 4
Abstract
Background: Tuberculosis outcome and clinical features of the infection are influenced by the degree of the multiplication of mycobacterias, host’s defense mechanisms and the organism’s capacity to fight through the antioxidant mechanisms against the aggression of the oxidative stress. The aim of the study was to assess the oxidative stress and inflammatory biomarkers in pulmonary tuberculosis. Material and methods: A prospective study, which included 46 patients with pulmonary tuberculosis and 36 healthy persons determined according to the clinical and biochemical criteria, was performed. The oxidative stress was assessed through the level of the advanced oxidation protein products, advanced glycation end-products, fibrinogen, amino acid catabolic products, activity of N-acetyl-β-D-glucosaminidase. The determination of the total antioxidant activity of plasma was performed through ABTS and CUPRAC methods. IL-8 and TNF-α were assessed using analysis kits of BOSTER (USA) producer. Results: Was established high level of the oxidative stress following the assessment of the concentration of the advanced oxidation protein products, advanced glycation end-products, fibrinogen, N-acetyl-β-D-glucosaminidase, urea and creatinine. High concentration of amino acid catabolic products was attributed to the nephrotoxic properties of the medication. Was identified high level of the plasma total antioxidant activity and antioxidant compounds. Cytokines concentration IL-8 and TNF-α was several times higher than in the control group and they were assessed as specific biomarkers. Conclusions: High level of the protein peroxidation, advanced glycation end-products, fibrinogen, protein catabolism compounds, pro-inflammatory cytokines – IL-8 and TNF-α confirmed the boosting of the oxidative stress. The elevated total antioxidant activity and antioxidant proteins demonstrated the organism’s capacity to redress the oxidative aggression.
Authors and Affiliations
Evelina Lesnic
Keywords
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- EP ID EP487929
- DOI 10.5281/zenodo.1106297
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