Abstract

Background/aim To evaluate total oxidant status (TOS), total antioxidant capacity (TAC), and paraoxonase 1 (PON1) levels in children with noncystic fibrosis (CF) bronchiectasis (BE), and to compare these levels with those of healthy controls. The study parameters were also evaluated according to some demographic, anthropometric, and clinical characteristics, as well as lung functions. Materials and methods Enrolled in the study were 118 children with non-CF BE and 68 healthy controls. Serum TOS, TAC, and PON1 levels were determined. Lung function tests were performed by spirometry. Results Serum TOS was higher in the patients [median 9.54 (IQR 25–75 = 7.05–13.30) µmol H2O2 Eq/L] than in the healthy subjects [6.64 (5.45–9.53) µmol H2O2 Eq/L] (P < 0.001). TAC was higher in patients with non-CF BE [1.07 (1.0–1.07) mmol Trolox Eq/L] than in the healthy controls [0.87 (0.77–0.98) mmol Trolox Eq/L] (P < 0.001). In addition, serum PON1 levels were significantly higher in the patients [106.5 (42.5–154.2) U/L] than in the controls [47.7 (27.5–82.1) U/L] (P < 0.001). The patients with low FEV1 had decreased TAC when compared to those who had normal FEV1 in non-CF BE. Conclusion The present study demonstrated that compared with the control group the children with non-CF BE had elevated oxidative status, antioxidant defenses parameters, and PON1 values.

Highlights

  • Bronchiectasis (BE) is a chronic airway disease characterized by abnormal destruction and dilatation of the large airways, bronchi, and bronchioles

  • total antioxidant capacity (TAC) was higher in patients with non-cystic fibrosis (CF) BE [1.07 (1.0–1.07) mmol Trolox Eq/L] than in the healthy controls [0.87 (0.77–0.98) mmol Trolox Eq/L] (P < 0.001)

  • The present study demonstrated that compared with the control group the children with non-CF BE had elevated oxidative status, antioxidant defenses parameters, and paraoxonase 1 (PON1) values

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Summary

Introduction

Bronchiectasis (BE) is a chronic airway disease characterized by abnormal destruction and dilatation of the large airways, bronchi, and bronchioles. In BE, airways are progressively damaged as a result of the interplay between chronic microbial infection, airway inflammation, and tissue-damaging substances secreted by neutrophils, eosinophils, macrophages, and epithelial cells, all of which produce proteinase enzymes and reactive oxygen radicals [2]. These radicals interact with various cellular components and macromolecules, and cause metabolic, structural, and functional damage that may lead to cell death [3].

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