Effect of REM sleep deprivation on the antioxidant status in the brain of wistar rats

Abstract

BackgroundRapid eye movement [REM] sleep deprivation is a stressor. It results in a predictable syndrome of physiological changes in rats. It has been proposed that reactive oxygen species and the resulting oxidative stress may be responsible for some of the effects of sleep deprivation.PurposeThe present study was undertaken to investigate the reversible nature of the effects of 96 hours of REM sleep deprivation on lipid peroxidation and total reduced glutathione level in the hypothalamus, midbrain and hindbrain of Wistar strain rats.MethodsThe rats were deprived of REM sleep using the inverted flowerpot technique. All the animals were maintained in standard animal house condition with 12-h light and 12-h dark cycles. At the end of the stipulated time Jugular venous blood sample of 2 ml was collected under mild ether anesthesia for the assay of stress index, plasma corticosterone. Lipid peroxidation using thiobarbituric acid, total reduced glutathione using DTNB (GSH) were assayed in the brain regions dissected out.ResultsThis study showed that 96 hours of REM sleep deprivation results in increased lipid peroxidation and reduction in total reduced glutathione level in the discrete regions of brain studied. However following restorative sleep for 24 hours all the changes reverts back to base line value. This study shows that oxidative stress produced by 96 hours of REM sleep deprivation is reversible.ConclusionFrom this study it is clear that, REM sleep deprivation is a potent oxidative stressor. This could probably play a role in the behavioral and performance alteration seen in both experimental animals as well as humans following REM sleep deprivation. Further investigations in this line are needed to highlight the importance of REM sleep.

“Rapid Eye Movement sleep deprivation of rat generates ROS in the hepatocytes and makes them more susceptible to oxidative stress”

“…Results published earlier also suggest that cytokines like tumor necrosis factor alpha (TNF-α ), IL-1β, and Interferon gamma (INF-γ) synergistically activate iNOS gene expression in the liver [35].…”

“…The stress response got alleviated to certain extent when rats were allowed to have recovery sleep. Other studies also indicate the increased oxidative stress in brain cells of rats after REMSD [21,34], reviewed in for animal models [35]. Conditions like obstructive sleep apnea in humans and rodents were also found to be positively correlated with increased ROS in the system [36,37], while Parkinson disease associated with REM sleep loss were also found to contribute to the colon oxidative stress and mitochondrial function [38].…”

Sleep duration is associated with sperm chromatin integrity among young men in Chongqing, China

“…Recently, certain indirect and direct clues have suggested that sleep duration can affect chromatin integrity, i.e. sleep restriction changed the level of reactive oxygen species which were important interruptors of chromatin structure (Alvarenga et al ., ; Lobascio et al ., ; Mathangi et al ., ; Novotny et al ., ; Villafuerte et al ., ). Moreover, a study on 26 human volunteers reported that sleep restriction disrupted the gene expresson of both circadian rhythm and the oxidative stress pathway, and chromatin modification was found to be affected in whole blood (Moller‐Levet et al ., ).…”

Insomnia in Peri- and Postmenopausal Women: Plasma Lipids, Lipid Peroxidation and Some Antioxidant System Parameters

“…Moreover, it has been shown that the lipids concentration might depends on the circadian system [6]. Also, experimental investigations has shown, that sleep loss may cause oxidative stress [7][8][9][10][11][12], which is a result of imbalance between free radicals production and antioxidant system activity [13]. These can lead to development of different cardiovascular [14], endocrine [15], mental [16], oncology [17] and other pathologies.…”