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Cell injury and repair resulting from sleep loss and sleep recovery in laboratory rats. Sleep 2014 Dec 01;37(12):1929-40



Pubmed ID


Pubmed Central ID




Scopus ID

2-s2.0-84914093940   50 Citations


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 N


Carol A. Everson PhD Professor in the Medicine department at Medical College of Wisconsin
Neil 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

Cell Death
Cell Proliferation
DNA Damage
DNA Repair
Disease Susceptibility
Glutathione Peroxidase
Intestine, Small
Organ Specificity
Oxidative Stress
Signal Transduction
Sleep Deprivation
jenkins-FCD Prod-482 91ad8a360b6da540234915ea01ff80e38bfdb40a