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Oxidative stress and its determinants in the airways of children with asthma
1Hacettepe University School of Medicine, Pediatric Allergy and Asthma Unit, AnkaraTurkey.
Insights
Childhood asthma significantly increases airway oxidative stress, indicated by higher malondialdehyde and lower glutathione levels. This oxidant/antioxidant imbalance is linked to asthma itself, not severity or specific antioxidant gene variants.
Area of Science:
- Pediatric Pulmonology
- Biochemistry
- Genetics
Background:
- Systemic oxidative stress is well-documented in childhood asthma.
- Limited data exists on airway-specific oxidant stress in pediatric asthma.
Purpose of the Study:
- To quantify airway oxidant/antioxidant imbalance in asthmatic children.
- To identify determinants of this imbalance, including asthma severity and antioxidant enzyme genotypes.
Main Methods:
- Collected exhaled breath condensate (EBC) from 110 mild asthmatics, 30 moderate asthmatics, and 191 healthy controls.
- Measured malondialdehyde (oxidative stress marker) and reduced glutathione (antioxidant marker) in EBC.
- Genotyped glutathione S transferase (GST) T1, GSTM1, and GSTP1 variants; analyzed risk factors using logistic regression.
Main Results:
- Asthmatic children exhibited significantly higher EBC malondialdehyde and lower reduced glutathione compared to controls (P < 0.001).
- No significant difference in oxidant/antioxidant markers was found between mild and moderate asthma groups.
- Asthma was the sole independent predictor of oxidative stress; antioxidant genotypes did not influence the oxidative burden.
Conclusions:
- Childhood asthma is strongly associated with significant airway oxidative stress.
- This oxidant burden is a characteristic of asthma, independent of disease severity or specific antioxidant gene variations.
Background:
There is ample evidence for the existence of a systemic oxidative stress in childhood asthma but relatively little information on the oxidant stress in the airways.
Objective:
To determine the extent of oxidant/antioxidant imbalance and describe its determinants in the airways of asthmatic children including asthma severity and the genotype of the antioxidant enzymes.
Methods:
One hundred and ten children with mild asthma, 30 children with moderate asthma and 191 healthy controls were included in the study. Exhaled breath condensate (EBC) was collected from all children with EcoScreen. Levels of malondialdehyde were measured as the indicator of oxidative stress, and of reduced glutathione as the indicator of antioxidant defense. Children were genotyped for the presence of null variants of glutathione S transferase (GST) T1 and GSTM1, and ile105val variant of GSTP1. Risk factors were analyzed with multivariate logistic regression.
Results:
EBC contained significantly higher levels of malondialdehyde and lower levels of reduced glutathione in asthmatic children compared with healthy controls (P < 0.001 for each), whereas there was no difference between mild and moderate asthmatics. Multivariate logistic regression identified asthma as the only independent factor contributing to oxidative stress. Genotypes of the antioxidant enzymes had no effect on the oxidative burden.
Conclusions:
Asthma is associated with an extremely powerful oxidative stress not only in the systemic circulation but also in the airways.
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