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.

Insights

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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