Oxidative stress is one of the pathophysiological pathways suggested for the development of cardiovascular diseases in obstructive sleep apnea. The recurrent nocturnal episodes of hypoxia/reoxygenation observed in patients with obstructive sleep apnea (OSA) appear to be partly responsible for the increased oxidative stress. We investigated the relationship between lipid peroxidation and DNA damage in OSA patients with or without metabolic syndrome (MetS). 117 patients that had recently diagnosed OSA with or without MetS, and 25 control subjects were studied. Plasma malondialdehyde (MDA) levels in fasting blood samples were measured by a high-performance liquid chromatography method and urine 8-hydroxydeoxyguanosine (8-OHdG) was accessed by a competitive ELISA kit method. The levels of MDA and 8-OHdG were significantly higher in total apnea patients than in the controls (P < 0.0001 and P < 0.005, respectively). Apnea patients with metabolic syndrome had slightly higher MDA and lower 8-OHdG levels than those in the patients without metabolic syndrome. The values of 8-OHdG was correlated with T%SaO2 < 90, T%SaO2 < %85, mean SaO2 (%), and the lowest SaO2 (%) (R = 0.511, P = 0.000, R = 0.420, P = 0.001, R = -0.448, P = 0.000, and R = -0.437, P = 0.001, respectively) in the severe apnea patients. Significant increases in the levels of MDA and 8-OHdG support the studies suggesting possible involvement of oxidative stress in OSA. According to the state of the MetS, there is no significant difference in the levels of oxidative stress markers in OSA patients with or without MetS. High correlations between 8-OHdG and oxygen saturation levels in severe apnea group indicate the role of hypoxia/reoxygenation in DNA damage.