Sleep deprivation under sustained hypoxia protects against oxidative stress.

TitleSleep deprivation under sustained hypoxia protects against oxidative stress.
Publication TypeJournal Article
Year of Publication2011
AuthorsRamanathan, L, Siegel JM
JournalFree radical biology & medicine
Volume51
Issue10
Pagination1842-8
Date Published2011 Nov 15
ISSN1873-4596
KeywordsAnimals, Anoxia, Biological Markers, Brain, Glucose, Glutathione, Hexokinase, Lipid Peroxidation, Male, Nitric Oxide, Oxidation-Reduction, Oxidative Stress, Protein Carbonylation, Rats, Rats, Sprague-Dawley, sleep deprivation, Superoxide Dismutase, Thiobarbituric Acid Reactive Substances
Abstract

We previously showed that total sleep deprivation increased antioxidant responses in several rat brain regions. We also reported that chronic hypoxia enhanced antioxidant responses and increased oxidative stress in rat cerebellum and pons, relative to normoxic conditions. In the current study, we examined the interaction between these two parameters (sleep and hypoxia). We exposed rats to total sleep deprivation under sustained hypoxia (SDSH) and compared changes in antioxidant responses and oxidative stress markers in the neocortex, hippocampus, brainstem, and cerebellum to those in control animals left undisturbed under either sustained hypoxia (UCSH) or normoxia (UCN). We measured changes in total nitrite levels as an indicator of nitric oxide (NO) production, superoxide dismutase (SOD) activity and total glutathione (GSHt) levels as markers of antioxidant responses, and levels of thiobarbituric acid-reactive substances (TBARS) and protein carbonyls as signs of lipid and protein oxidation products, respectively. We found that acute (6h) SDSH increased NO production in the hippocampus and increased GSHt levels in the neocortex, brainstem, and cerebellum while decreasing hippocampal lipid oxidation. Additionally, we observed increased hexokinase activity in the neocortex of SDSH rats compared to UCSH rats, suggesting that elevated glucose metabolism may be one potential source of the enhanced free radicals produced in this brain region. We conclude that short-term insomnia under hypoxia may serve as an adaptive response to prevent oxidative stress.

DOI10.1111/j.1365-2869.2012.01023.x
Alternate JournalFree Radic. Biol. Med.