Cell injury and repair resulting from sleep loss and sleep recovery in laboratory rats. Sleep 2014 Dec 01;37(12):1929-40
Date
10/18/2014Pubmed ID
25325492Pubmed Central ID
PMC4548518DOI
10.5665/sleep.4244Scopus ID
2-s2.0-84914093940 (requires institutional sign-in at Scopus site) 89 CitationsAbstract
STUDY OBJECTIVES: Increased cell injury would provide the type of change in constitution that would underlie sleep disruption as a risk factor for multiple diseases. The current study was undertaken to investigate cell injury and altered cell fate as consequences of sleep deprivation, which were predicted from systemic clues.
DESIGN: Partial (35% sleep reduction) and total sleep deprivation were produced in rats for 10 days, which was tolerated and without overtly deteriorated health. Recovery rats were similarly sleep deprived for 10 days, then allowed undisturbed sleep for 2 days. The plasma, liver, lung, intestine, heart, and spleen were analyzed and compared to control values for damage to DNA, proteins, and lipids; apoptotic cell signaling and death; cell proliferation; and concentrations of glutathione peroxidase and catalase.
MEASUREMENTS AND RESULTS: Oxidative DNA damage in totally sleep deprived rats was 139% of control values, with organ-specific effects in the liver (247%), lung (166%), and small intestine (145%). Overall and organ-specific DNA damage was also increased in partially sleep deprived rats. In the intestinal epithelium, total sleep deprivation resulted in 5.3-fold increases in dying cells and 1.5-fold increases in proliferating cells, compared with control. Recovery sleep restored the balance between DNA damage and repair, and resulted in normal or below-normal metabolic burdens and oxidative damage.
CONCLUSIONS: These findings provide physical evidence that sleep loss causes cell damage, and in a manner expected to predispose to replication errors and metabolic abnormalities; thereby providing linkage between sleep loss and disease risk observed in epidemiological findings. Properties of recovery sleep include biochemical and molecular events that restore balance and decrease cell injury.
Author List
Everson CA, Henchen CJ, Szabo A, Hogg NAuthors
Carol A. Everson PhD Professor in the Medicine department at Medical College of WisconsinNeil Hogg PhD Associate Dean, Professor in the Biophysics department at Medical College of Wisconsin
Aniko Szabo PhD Professor in the Institute for Health and Equity department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsAntioxidants
Catalase
Cell Death
Cell Proliferation
DNA Damage
DNA Repair
Disease Susceptibility
Glutathione Peroxidase
Intestine, Small
Liver
Lung
Male
Organ Specificity
Oxidative Stress
Rats
Signal Transduction
Sleep
Sleep Deprivation
