Advanced oxidation protein products and ischaemia- modified albumin in obstructive sleep apnea Serkan Ozben * , Nergiz Huseyinoglu † , Ferhat Hanikoglu ‡ , Tolga Sinan Guvenc § , Binnaz Zeynep Yildirim ¶ , Aysegul Cort ‡ , Sebahat Ozdem ‡ and Tomris Ozben ‡ * Department of Neurology, Bakirkoy Training and Research Hospital for Psychiatry, Neurology and Neurosurgery Diseases, Istanbul, † Department of Neurology, Medical Faculty Kafkas University, Kars, ‡ Department of Biochemistry, Medical Faculty Akdeniz University, Antalya, § Department of Cardiology, Medical Faculty, Kafkas University, Kars, ¶ Department of Respiratory Diseases, Medical Faculty Medipol University, Istanbul, Turkey ABSTRACT Background Several studies have shown that obstructive sleep apnea increases incidence of cardiovascular morbidity and mortality. The high systemic oxidative stress in obstructive sleep apnea has been considered as a major pathogenic mechanism leading to cardiovascular disease. Oxidative stress-related lipid and DNA oxidation in obstructive sleep apnea have been reported in the previous studies. In contrast, there is limited and con- tradictory information regarding protein oxidation in obstructive sleep apnea patients such as ischaemia-modi- fied albumin and advanced oxidation protein products. Therefore, we aimed to investigate plasma ischaemia- modified albumin and advanced oxidation protein products and their correlation with total oxidative status and total antioxidative capacity in the obstructive sleep apnea patients. Methods Plasma ischaemia-modified albumin, advanced oxidation protein products, total oxidative status and total antioxidative capacity were measured in 25 healthy volunteers and 59 obstructive sleep apnea patients diagnosed with polysomnography. Results Plasma total antioxidative capacity was significantly lower (P = 0012) and total oxidative status was significantly higher (P < 0001) in the patients compared to the controls demonstrating increased oxidative stress in the patients. Plasma advanced oxidation protein products were significantly higher in the patients than the controls (P = 0024). Plasma ischaemia-modified albumin levels were not statistically different between the obstructive sleep apnea patients and controls (P = 074). Conclusions We conclude that high systemic oxidative stress in obstructive sleep apnea is reflected by increased advanced oxidation protein products without causing an increase in ischaemia-modified albumin. Keywords Advanced oxidation protein products, ischaemia-modified albumin, obstructive sleep apnea, oxidative stress, total antioxidative capacity, total oxidative status. Eur J Clin Invest 2014; 44 (11): 1045–1052 Introduction Obstructive sleep apnea (OSA) is a condition characterized by cessation of respiration due to obstruction of the upper airway during sleeping [1–4]. Its prevalence is approximately 4% in males and 2% in females in the adult population [1,2]. It is seen frequently in patients with morbid obesity, cardiac, neurologi- cal, renal and respiratory diseases [1,3]. In OSA, each episode of airway obstruction is followed by decreased arterial oxygen (O 2 ) saturation. Intermittent hypoxia and hypoxia/reoxygenation sequences causing increased pro- duction of ROS in OSA patients are associated with increased cardiovascular risk and mediated by several intermediary mechanisms such as oxidative stress and sympathetic activa- tion [2–5]. Increased levels of ROS in the OSA patients may result in oxidative damage to proteins, lipids and DNA. Oxidative damage to proteins might lead more devastating results than damage to lipids and DNA. Protein oxidation is a relevant marker of oxidative stress as plasma proteins are critical targets for oxidants. Oxidative protein damage causes irreversible modifications in proteins. The structure and activity of oxidized proteins change profoundly in comparison with their native forms. Oxidative modification of proteins in vivo may affect a variety of cellular functions [6–9]. Advanced oxidation protein products (AOPP) are formed during oxidative stress and exert European Journal of Clinical Investigation Vol 44 1045 DOI: 10.1111/eci.12338 ORIGINAL ARTICLE