DNA Damage in Children With Obstructive Adenotonsillar Hypertrophy Ozgur Yoruk, MD,* Hakan Alp, MD,† Sancak Yuksel, MD,‡ and Ebubekir Bakan, MD§ Abstract: The objective of this prospective, controlled study was to evaluate oxidative DNA damage in children with obstructive adenotonsillar hypertrophy. This study included 30 patients with ob- structive adenotonsillar hypertrophy (male/female ratio, 3:2; age range, 3–9 y) scheduled to undergo tonsillectomy and adenoidectomy and 25 control subjects of similar age and sex with no adenotonsillar disease or airway obstruction. Urine and blood samples were obtained from each child for 8-hydroxy 2-deoxyguanosine (8-OhdG) and malondialdehyde (MDA) concentrations. There were significant dif- ferences in leukocyte (3.28 [0.69/10 6 ] vs 0.70 [0.15/10 6 ] dG) and urine 8-OhdG (8.22 [2.27/10 6 ] vs 5.26 [1.3/10 6 ] dG) levels in patients with obstructive adenotonsillar hypertrophy and healthy subjects (P < 0.001 for both). Plasma (2.98 [1.31] vs 1.14 [0.64] μM) and urine (1.77 [0.84] vs 0.56 [0.32] μM) MDA levels were also different (P < 0.001 for both). There were positive correlations between 8-OhdG in leukocyte DNA and plasma MDA (r = 0.648, P < 0.001) and be- tween levels of urine 8-OhdG excretion and urine MDA (r = 0.588, P < 0.001). The DNA damage in children with adenotonsillar hyper- trophy should be kept in mind, but further studies must be done with larger patient groups. Key Words: Obstructive adenotonsillar hypertrophy, DNA damage, 8-hydroxy 2-deoxyguanosine, malondialdehyde (J Craniofac Surg 2014;25: 2156–2159) A denotonsillar hypertrophy in children can lead to narrowing or obstruction of the upper airway. Thus, snoring is a common complaint among these children due to breathing through the mouth. 1 Adenotonsillectomy is a potentially frequent surgical proce- dure performed on children by otolaryngologists. Adenotonsillar diseases have received a lot of attention in recent years related to their pathologic, clinical, and immunologic attributes. 2 Obstructive adenotonsillar hypertrophy (OAH) is a childhood disease and is identified by hypoxia/reoxygenation periods. 3,4 It may lead to insta- bility between antioxidant defence mechanisms and reactive oxygen species (ROS). Although the cellular mechanisms of oxygen toxic- ity are not yet fully understood, oxidative impairment of cellular el- ements by the increased generation of ROS is the most likely pathway by which excessive concentrations of oxygen impair the cells. 2 Excep- tionally excessive levels of ROS due to overproduction/insufficient elimination can harm cellular membrane lipids, proteins, and nucleic acids. 2 Oxidation of cell membrane lipids mediated by ROS causes lipid peroxidation products. Lipid peroxides induce a well-understood path- way of cellular harm in humans; their existence points toward oxidative destruction in tissues and cells. Lipid peroxides are both modifiable and may turn into a composite series of elements. These involve responsive carbonyl compounds, among which malondialdehyde (MDA) is the most plentiful. Thus, the measurement of MDA is extensively used as an indicator of lipid peroxidation. 5 Oxidative damage upsets biomolecules other than lipids— notably proteins and DNA. The ROS lead to breakage in DNA he- lices and base mutations and oxidative damage to the guanine bases. As 8-hydroxy 2-deoxyguanosine (8-OhdG) resulting from oxida- tion of guanine residues, it can act as an accurate biomarker of ox- idative DNA damage. 6 Current studies have shown remarkably raised levels of 8-OHdG in a number of systemic diseases. 7,8 The amounts of oxidation products of DNA structure in biologic tissues and fluids (eg, urine, serum) have been shown to be trustworthy markers of oxidative stress. 9 In this study, we aimed to investigate the levels of these oxi- dant damage markers in children with OAH, using 8-OHdG levels in leukocyte DNA and urine samples as a marker of oxidative dam- age to DNA as well as plasma and urine MDA levels as the index of lipid peroxidation. MATERIALS AND METHODS Patients Fifty-five children were included in this study. Study groups were selected among the patients who were admitted to the otolar- yngology unit of our hospital. Institutional ethics committee ap- proval was obtained (protocol number, B.30.2.ATA.0.01.00/53). The study consisted of a patient group (30 children with OAH) and a control group (25 children of similar sex and age). The age range was 3 to 9 years (mean age, 5 y). The male/female ratio was 3:2. All of the patients had a diagnosis of OAH and were scheduled to undergo tonsillectomy with adenoidectomy. They were selected by physical and endoscopic examination and history. After a complete general inspection and ear-nose-throat ex- amination, rigid and flexible endoscopic examination was per- formed for the assessment of adenoid size and nasal patency. Lateral skull radiography was used for imaging the nasopharyngeal air passage. According to Brodsky criteria, the size of the tonsils was graded from I to IV (grade I, tonsils are hidden tonsillar fossa; grade II, tonsils extend half of the way to the midline; grade III, ton- sils are extending three quarters of theway to the midline; grade IV, From 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; ‡De- partment of Otorhinolaryngology-Head & Neck Surgery, University of Texas Medical School at Houston, Houston, Texas; and §Medical Fac- ulty, Department of Biochemistry, Ataturk University, Erzurum, Turkey. Received April 15, 2014. Accepted for publication June 19, 2014. Address correspondence and reprint requests to Ozgur Yoruk, MD, Tıp Fakültesi, Atatürk Üniversitesi, Kulak Burun Boğaz ABD, 25100 Erzurum, Turkey; E-mail: dryoruk_40@hotmail.com Presented at the 2012 Annual Meeting of the American Academy of Otolaryngology-Head and Neck Surgery, Washington, DC. The authors report no conflicts of interest. Copyright © 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000001158 CLINICAL STUDY 2156 The Journal of Craniofacial Surgery • Volume 25, Number 6, November 2014 Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.