DNA methylation and oxidative stress in sleep deprived rats

Objective: Sleep deprivation and poor quality of sleep are a current issue in our society. In animal models, sleep deprivation can induce diverse alterations, including oxidative stress in several organs. A highly active hydroxyl radical can break the DNA strands generating 8-hydroxy-2-deoxyguanosine (8-OHdG). Thus, this DNA damage may compromise gene expression. Another factor that can alter gene expression is the DNA methylation, which is associated with transcription control. Considering these observations the aim of this study was to evaluate if sleep deprivation in rats could lead to DNA oxidative damage and if DNA methylation pattern could be changed by sleep deprivation. Methods: A group of male Wistar rats were submitted to the sleep deprivation procedure for 96h (Sleep-Deprived - SD) by the classical platform method; another group of animals were put individually into the same container as the sleep-deprived animals, but the water was substituted by wood paring (Control - CT); and the last group, where the animals were allowed to sleep 24h after the sleep deprivation (Rebound - RB). After the experimental procedure, animals were euthanized. Serum and whole blood were collected to quantify 8-OHdG and global DNA methylation. Results: Analyzing serum 8-OHdG, global methylation and global/CpG islands methylation ratio, we found no differences when comparing the experimental and CT groups. Analyzing CpG islands methylation we found a decrease of methylation at the islands on SD group compared with CT group and at the RB group this alteration did not returned to basal levels. Conclusion: The decrease in CpG islands methylation could modulate an altered gene expression as a consequence of sleep deprivation and sleep recovery.