Background and objective: The aim of this study was to investigate the mechanism by which oxidative stress induced by chronic intermittent hypoxia (IH) causes myocardial damage in obstructive sleep apnoea syndrome.
Methods: A total of 160 Wistar rats were divided into five experimental groups and subjected to chronic IH with different concentrations of oxygen (5%, 7.5%, 10% IH groups; 10% continuous oxygen and normoxia control groups). Eight rats from each group were sacrificed at the 2-, 4-, 6- and 8-week time points. Superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels and total anti-oxidant capability (T-AOC) were measured in supernatants of heart homogenates. Expression of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, p22phox and NOX2, and thioredoxin-2 (Trx-2) genes were determined by measuring messenger RNA (mRNA) levels by real-time polymerase chain reaction.
Results: Compared with the control groups, MDA levels increased over time in the IH groups, whereas T-AOC and SOD activity decreased over time. MDA, T-AOC and SOD activity peaked at 6 weeks into the IH treatment. The 5% IH group showed significantly higher expression of p22phox and thioredoxin-2 mRNA, as compared with the other IH groups, as well as the control groups.
Conclusions: The severity of oxidative stress induced by chronic IH in myocardial tissue was significantly correlated with the degree of IH. NADPH oxidase and Trx-2 are important mediators of oxidative stress induced by IH.