• Peter Celec, Július Hodosy, Michal Behuliak, Roland Pálffy, Roman Gardlík, Lukáč Halčák, and Imrich Mucska.
• Institute of Molecular Biomedicine, Comenius University, Sasinkova 4, 811 08, Bratislava, Slovakia. petercelec@gmail.com
• Sleep Breath. 2012 Jun 1; 16 (2): 393-8.

PurposeThe pathogenesis of cardiovascular complications of obstructive sleep apnea syndrome (OSAS) can be explained by oxidative and carbonyl stress due to oxygenation and reoxygenation injury during sleep. This hypothesis has yet to be proved experimentally, although several clinical observations have found increased oxidative damage in plasma. Continuous positive airway pressure (CPAP) improves symptoms and prognosis of patients with OSAS.MethodsPatients with confirmed SAS (n = 89) underwent polysomnography and received CPAP treatment. Plasma and saliva samples were taken before CPAP therapy as well as after 1 and 6 months of CPAP treatment. Selected markers of oxidative and carbonyl stress were measured in plasma and saliva, and their dynamics was statistically analyzed.ResultsPlasma levels of thiobarbituric acid reacting substances-a marker of lipoperoxidation-and advanced glycation end products (AGEs)-a marker of carbonyl stress-were decreased by the CPAP therapy. The decrease of AGEs and fructosamine was also found in saliva. Interestingly, no gender differences and no changes of antioxidant status measured as total antioxidant capacity and ferrous reducing ability were found in either of the samples.ConclusionPrevious findings of lowered plasma markers of oxidative stress were confirmed. Plasma AGEs were lowered by CPAP therapy. This is the first study analyzing markers of oxidative and carbonyl stress in saliva. Non-invasive sampling of saliva makes it a very interesting source of information for repeated monitoring of therapy success. Salivary AGEs and fructosamine as markers of carbonyl stress were decreased by the CPAP therapy and might therefore have potential informative value for clinical observations, as well as for the understanding of the pathogenesis of OSAS complications.

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