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Published on: June 14, 2020
DNA damage in children with obstructive adenotonsillar hypertrophy
Ozgur Yoruk1, Hakan Alp, Sancak Yuksel
1From the *Medical Faculty, Department of Otolaryngology and Head and Neck Surgery, Ataturk University, Erzurum, Turkey; †Medical Faculty, Department of Biochemistry, Yuzuncu Yıl University, Van, Turkey; ‡Department of Otorhinolaryngology-Head & Neck Surgery, University of Texas Medical School at Houston, Houston, Texas; and §Medical Faculty, Department of Biochemistry, Ataturk University, Erzurum, Turkey.
Children with obstructive adenotonsillar hypertrophy show increased oxidative DNA damage, indicated by higher levels of 8-hydroxy 2-deoxyguanosine (8-OhdG) and malondialdehyde (MDA). This suggests a link between airway obstruction and cellular damage in pediatric patients.
Area of Science:
- Pediatric Medicine
- Biochemistry
- Genetics
Background:
- Obstructive adenotonsillar hypertrophy is a common condition in children.
- Oxidative stress is implicated in various chronic diseases.
- Assessing DNA damage can provide insights into disease pathogenesis.
Purpose of the Study:
- To investigate oxidative DNA damage in children diagnosed with obstructive adenotonsillar hypertrophy.
- To compare levels of specific oxidative stress biomarkers between affected children and healthy controls.
Main Methods:
- Prospective, controlled study design.
- Inclusion of 30 children with obstructive adenotonsillar hypertrophy and 25 age-matched controls.
- Analysis of urine and blood samples for 8-hydroxy 2-deoxyguanosine (8-OhdG) and malondialdehyde (MDA) concentrations.
Main Results:
- Significantly elevated leukocyte and urine 8-hydroxy 2-deoxyguanosine (8-OhdG) levels in patients compared to controls (P < 0.001).
- Significantly higher plasma and urine malondialdehyde (MDA) levels were observed in patients (P < 0.001).
- Positive correlations found between leukocyte DNA 8-OhdG and plasma MDA, and between urine 8-OhdG and urine MDA.
Conclusions:
- Children with obstructive adenotonsillar hypertrophy exhibit increased oxidative DNA damage.
- The findings highlight the potential role of oxidative stress in the pathophysiology of this condition.
- Further research with larger cohorts is warranted to confirm these results.
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