Effects of various degrees of oxidative stress induced by intermittent hypoxia in rat myocardial tissues

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, p22^phox 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 p22^phox 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.