Objectives: 

Obstructive sleep apnoea (OSA) refers to repetitive episodes of upper airways obstruction which occur during sleep time. OSA generates a cohort of cardiovascular, metabolic and neuropsychiatric pathologies to conform the obstructive sleep apnoea syndrome (OSAS). Since each obstruction produces a fall in PO2 and haemoglobin saturation, intermittent hypoxia (IH) and associated oxidative stress are proposed to be at the core of OSAS pathologies. Yet, some authors found that humans with OSAS and animals exposed to IH do not exhibit redox status alterations, consequently the oxidative stress-OSAS associated pathologies linkage is not universally accepted. Literature discrepancies could be due to: a) the heterogeneity on the level of lowest oxygen saturation, both in patients and IH animal models, and; b) the use of inadequate biomarkers of oxidative damage. In present work we have aimed to define if IH does indeed produce an oxidative status and its putative association with dislipaemias.

Materials: 

We have used adult male Wistar rats subjected to IH of two intensities. Protocol for IH was: 10 or 5% O2, 40s/ 21% O2, 80s, 8h/day, 15 days. We measured reduced and oxidized glutathione and lipid peroxides levels, aconitase and fumarase activity ratios, and the glutathione peroxidase, catalase, and cytoplasmic and mitochondrial superoxide dismutase activities in several tissues, liver levels of nuclear NFkBp65, and plasma lipid levels.

Results: 

Low and high IH intensity caused lowest oxygen saturations of 91.7  0.8 and 73.5  1.4%, respectively. Redox parameters indicate that IH generates a pro-oxidative status that reaches the level of frank oxidative stress with the most intense hypoxia. An additional finding is that oxidative damage is tissue specific. Nuclear NFkBp65 augments in parallel to IH intensity.

Conclusions: 

Finally, IH caused an increase in plasma triglycerides and total cholesterol which are related to lowest oxygen saturation.