OBJECTIVE: Several studies suggest that obstructive sleep apnea syndrome (OSAS) is associated with oxidative stress. However, there are also contrary observations and the role of antioxidant mechanisms has not been fully explored. PATIENTS AND METHODS: The present study evaluated serum total antioxidant status (TAS) in 32 OSAS patients without comorbidities, before and after a diagnostic sleep study and at a second sleep study after continuous positive airway pressure (CPAP) application. RESULTS: Lower TAS values were found in the morning, immediately after the first sleep study, compared with those before sleep (1.68 ± 0.11 vs. 1.61 ± 0.10 mmol/l, p < 0.01); this was evident in patients with less severe syndrome [apnea-hypopnea index (AHI) <30; 1.73 ± 0.08 vs. 1.65 ± 0.09 mmol/l, p = 0.01] but not in severe syndrome (AHI ≥30; 1.64 ± 0.12 vs. 1.58 ± 0.10 mmol/l, p = 0.07). After CPAP application, a statistically significant decrease in TAS values was observed in patients with less severe syndrome (1.72 ± 0.05 vs. 1.63 ± 0.04 mmol/l, p = 0.003). On the contrary, no statistically significant changes in TAS were observed in patients with severe syndrome. CONCLUSIONS: The present study supports a reduction in antioxidant capacity during sleep in otherwise healthy patients with OSAS. This reduction was evident in less severe syndrome. However, a single night of CPAP application seems to ameliorate this antioxidant disturbance only in less severe syndrome.
OBJECTIVE: Several studies suggest that obstructive sleep apnea syndrome (OSAS) is associated with oxidative stress. However, there are also contrary observations and the role of antioxidant mechanisms has not been fully explored. PATIENTS AND METHODS: The present study evaluated serum total antioxidant status (TAS) in 32 OSAS patients without comorbidities, before and after a diagnostic sleep study and at a second sleep study after continuous positive airway pressure (CPAP) application. RESULTS: Lower TAS values were found in the morning, immediately after the first sleep study, compared with those before sleep (1.68 ± 0.11 vs. 1.61 ± 0.10 mmol/l, p < 0.01); this was evident in patients with less severe syndrome [apnea-hypopnea index (AHI) <30; 1.73 ± 0.08 vs. 1.65 ± 0.09 mmol/l, p = 0.01] but not in severe syndrome (AHI ≥30; 1.64 ± 0.12 vs. 1.58 ± 0.10 mmol/l, p = 0.07). After CPAP application, a statistically significant decrease in TAS values was observed in patients with less severe syndrome (1.72 ± 0.05 vs. 1.63 ± 0.04 mmol/l, p = 0.003). On the contrary, no statistically significant changes in TAS were observed in patients with severe syndrome. CONCLUSIONS: The present study supports a reduction in antioxidant capacity during sleep in otherwise healthy patients with OSAS. This reduction was evident in less severe syndrome. However, a single night of CPAP application seems to ameliorate this antioxidant disturbance only in less severe syndrome.
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