Sleep deprivation and cellular responses to oxidative stress.
OBJECTIVE
It has been hypothesized that sleep deprivation represents an oxidative challenge for the brain and that sleep may have a protective role against oxidative damage. This study was designed to test this hypothesis by measuring in rats the effects of sleep loss on markers of oxidative stress (oxidant production and antioxidant enzyme activities) as well as on markers of cellular oxidative damage (lipid peroxidation and protein oxidation).


METHODS
The analyses were performed in the brain and in peripheral tissues (liver and skeletal muscle), after short-term sleep deprivation (8 hours), after long-term sleep deprivation (3-14 days), and during recovery sleep after 1 week of sleep loss. Short-term sleep deprivation was performed by gentle handling; long-term sleep deprivation was performed using the disk-over-water method.


METHODS
Sleep research laboratory at University of Wisconsin-Madison.


METHODS
Adult male Wistar Kyoto rats (n = 69) implanted for polygraphic (electroencephalogram, electromyogram) recording.


RESULTS
Aliquots of brain, liver, or skeletal muscle homogenate were used to assess oxidant production, superoxide dismutase activity, lipid peroxidation, and protein oxidation. No evidence of oxidative damage was observed at the lipid and/or at the protein level in long-term sleep-deprived animals relative to their yoked controls, nor in the cerebral cortex or in peripheral tissues. Also, no consistent change in antioxidant enzymatic activities was found after prolonged sleep deprivation, nor was any evidence of increased oxidant production in the brain or in peripheral tissues.


CONCLUSIONS
The available data do not support the assumption that prolonged wakefulness may cause oxidative damage, nor that it can represent an oxidative stress for the brain or for peripheral tissue such as liver and skeletal muscle.
Gopalakrishnan
Anupama
A
Department of Psychiatry, University of Wisconsin, Madison 53719, USA.
Ji
Li Li
LL
Cirelli
Chiara
C
D000818:Animals; D015415:Biomarkers; D001921:Brain / Q000166:cytology* / Q000378:metabolism*; D004569:Electroencephalography; D004576:Electromyography; D004791:Enzyme Inhibitors / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D016877:Oxidants / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012892:Sleep Deprivation / Q000378:metabolism*; D012895:Sleep, REM / Q000502:physiology; D019810:Sodium Azide / Q000494:pharmacology; D013050:Spectrometry, Fluorescence; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors; D014851:Wakefulness / Q000502:physiology
D015415:Biomarkers; D004791:Enzyme Inhibitors; D016877:Oxidants; D019810:Sodium Azide; D013482:Superoxide Dismutase