Cell Injury and Repair Resulting from Sleep Loss and Sleep Recovery in Laboratory Rats
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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.
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In rats, myeloperoxidase activity in the intestines was increased after recovery sleep compared with baseline and sleep-deprivation levels, suggesting ongoing reactive processes during recovery sleep subsequent to sleep deprivation.
“However, myeloperoxidase activity in the intestines was increased after recovery sleep compared with baseline and sleep-deprivation levels, suggesting ongoing reactive processes during recovery sleep subsequent to sleep deprivation (174).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [174]
In rats, 48 h of recovery sleep following 10 days of sleep deprivation restored sleep deprivation-induced increases of myeloperoxidase activity in the lung and liver.
“In rats, 48 h of recovery sleep following 10 days of sleep deprivation restored sleep deprivation-induced increases of myeloperoxidase activity (an enzyme constituent of neutrophils) in the lung and liver.”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [174]
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The Sleep-Immune Crosstalk in Health and Disease
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“In this study, cell injury was most pronounced in the intestine (173), which could result in increased intestinal permeability (leaky gut) and, together with the impairment of host defense following sleep loss, to a translocation of commensal bacteria and PAMP-driven systemic inflammation (175, 303) (see also sect.”
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- Authors
- Everson, C. A., Henchen, C. J., Szabo, A., & Hogg, N.
- Affiliations
- Medical College of Wisconsin (US)
- Department of Population Health, The Medical College of Wisconsin, Milwaukee, WI
- Corresponding author
- Everson, Carol A.
- Venue
- Sleep
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-12-01
- Volume
- 37
- Issue
- 12
- Pages
- 1929-1940
- ISSN
- 0161-8105 (ISSN-L)
- 1550-9109
- PMC
- PMC4548518
- OpenAlex
- W2331378898
- Cited by
- 136
- References
- 90
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 12 · 2023: 16 · 2022: 10 · 2021: 10 · 2020: 10 · 2019: 15 · 2018: 11 · 2017: 7 · 2016: 11 · 2015: 5
- FWCI
- 10.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- SLEEP (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs
- Vanderbilt University
- Medical College of Wisconsin
- National Institutes of Health (UL1TR000055)
- National Heart, Lung, and Blood Institute (HL086447, R01HL086447, R01HL080744, HL080744)
- National Center for Advancing Translational Sciences
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- sleep deprivation, sleep recovery, cell damage, oxidative DNA damage, apoptosis, cell proliferation, intestinal epithelium, oxidative stress, glutathione peroxidase, catalase, liver, lung, small intestine, heart, spleen
- MeSH terms
- Animals, Antioxidants, Catalase, Disease Susceptibility, DNA Damage, DNA Repair, Glutathione Peroxidase, Intestine, Small, Liver, Lung, Male, Organ Specificity, Sleep, Sleep Deprivation, Signal Transduction, Cell Death, Oxidative Stress, Cell Proliferation, Rats
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