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 Radic Biol Med
Date Published2011 Nov 15
KeywordsAnimals, Anoxia, Biomarkers, 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

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.

Alternate JournalFree Radic. Biol. Med.
PubMed ID21907278
PubMed Central IDPMC3197752
Grant ListI01 BX001753 / BX / BLRD VA / United States
MH64109 / MH / NIMH NIH HHS / United States
NS14610 / NS / NINDS NIH HHS / United States
R01 DA034748 / DA / NIDA NIH HHS / United States
R01 MH064109 / MH / NIMH NIH HHS / United States
R01 MH064109-09 / MH / NIMH NIH HHS / United States
R01 NS014610 / NS / NINDS NIH HHS / United States
R01 NS014610-30 / NS / NINDS NIH HHS / United States