Sleep deprivation decreases superoxide dismutase activity in rat hippocampus and brainstem

Ramanathan, Lalini; Gulyani, Seema; Nienhuis, Robert; Siegel, Jerome M.

doi:10.1097/00001756-200208070-00007

Cited by 226 publications

(168 citation statements)

References 20 publications

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“…As changes in protein phosphorylation occur within minutes and are associated with alterations in cellular activities [Shaw et al, 1995;Asthagiri et al, 1999;King et al, 2006;Morii et al, 2006;Nunez Rodriguez et al, 2006], our results provide evidence that such alterations occur within the time frames associated with individual sleep-wake bouts in rats [Timo-Iaria et al, 1970;Tobler and Borbely, 1986]. In addition, these data are consistent with previous reports that examined regional phosphorylated protein expression by immunohistochemical methods [Cirelli and Tononi, 1998], levels of specific phosphoproteins [Guan et al, 2004;Basheer et al, 2005;Naidoo et al, 2005;Bandyopadhya et al, 2006;Davis et al, 2006], or enzymatic activities [Ramanathan et al, 2002;Mackiewicz et al, 2003;Naidoo et al, 2005] following SD. …”

supporting

confidence: 91%

“…GSTs are a multi-gene family of proteins that are associated with the maintenance of cellular oxidationreduction [Pocernich et al, 2000;Zhu et al, 2006]. The failure to maintain the cellular oxidation state has been proposed to account for some of the deleterious effects of SD [D'Almeida et al, 1998;Ramanathan et al, 2002] and has long been associated with the detrimental effects of aging [Zhu et al, 2006]. It is interesting to note that an increase in gst pi 2 subunit mRNA was also reported following spontaneous sleep [Cirelli et al, 2004].…”

Section: Protein Expression Across Spontaneous Sleep-wakefulness Jourmentioning

confidence: 99%

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Rapid alterations in cortical protein profiles underlie spontaneous sleep and wake bouts

Vázquez

Hall

Witkowska

et al. 2008

J of Cellular Biochemistry

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Existing data indicate that sleep-wakefulness is an essential behavior. The biological function(s) of sleep, however, remains unknown, due, in part, to the lack of information available at the intracellular level. Preliminary microarray analyses show that changes in behavioral state influence regional mRNA profiles; however, the impact of sleep on protein signatures is virtually unexplored. In these studies, cortical protein profiles were examined after timed bouts of spontaneous sleep-wakefulness. Within minutes of each behavioral state examined, a small number of spots showing unique expression were detected. Mass spectroscopy analyses of sleep-and wake-related spots identified proteins associated with multiple functional categories. Two sleep-associated proteins were further validated using a sleep deprivation paradigm. We found preliminary evidence for two different post-transcriptional mechanisms-one (GAPDH) in which the amount of protein was increased in the recovery sleep following prolonged waking, while the other (actin) suggested that post-translational modifications may underlie sleep. The similarities between the effects of sleep on both protein and mRNA profiles indicate that dynamic intracellular changes underlie sleep-wake states and are consistent with roles for sleep in multiple biological functions. J. Cell. Biochem. 105: 1472Biochem. 105: -1484Biochem. 105: , 2008. ß 2008 Wiley-Liss, Inc. KEY WORDS: TWO-DIMENSIONAL ELECTROPHORESIS (2DE); MASS SPECTROMETRY; SPONTANEOUS SLEEP-WAKE BOUTS; SLEEP-ASSOCIATED PROTEIN EXPRESSIONS leep-wake behavior is a complex and tightly regulated Achermann, 1999, 2000] amalgam of physiological processes that involves reciprocal interactions between numerous brain regions that is coordinated by multiple neurotransmitter/peptide systems [Lin, 2000;Jones, 2004]. Sleep is exhibited by all animals studied thus far [Campbell and Tobler, 1984;Tobler, 2000] and constitutes a significant percentage of a 24 h period [Carskadon and Dement, 2000;Ohayon et al., 2004]. Alternations between sleep and wakefulness are regulated by a combination of circadian (sleep timing) [Edgar, 1995] and homeostatic factors (sleep need) [Borbely, 1982]. The homeostatic regulation of sleep is based on the observation that following sleep deprivation (SD), there is an increase in sleep time and intensity that is proportional to the sleep lost, suggesting that a need for sleep accumulates during waking in both rodents and humans [Tobler and Borbely, 1986;Riedner et al., 2007;Vyazovskiy et al., 2007]. In humans, SD results in marked cognitive and physiological impairments [Drummond and Brown, 2001;Durmer and Dinges, 2005], while prolonged SD in rats [Rechtschaffen, 1998] and flies [Shaw et al., 2002] is fatal. The biological function(s) of sleep, however, remains poorly characterized, though most agree that sleep serves a restorative function [Benington and Heller, 1995]. Proposed roles for sleep include the maintenance of body temperature [McGinty and Szymusiak, 1990;Wehr, 1992], energy ...

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supporting

confidence: 91%

Section: Protein Expression Across Spontaneous Sleep-wakefulness Jourmentioning

confidence: 99%

Rapid alterations in cortical protein profiles underlie spontaneous sleep and wake bouts

Vázquez

Hall

Witkowska

et al. 2008

J of Cellular Biochemistry

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“…This has been supported by animal studies where sleep loss caused oxidative damage in the brain (Ramanathan et al, 2002, Suer et al, 2011 and increased lipid peroxidation (Thamaraiselvi et al, 2012). However, some animal studies have found that one to two weeks of sleep deprivation had no effect on oxidative stress in any brain region, including protein oxidation and lipid peroxidation (D'Almeida et al, 1997, Gopalakrishnan et al, 2004).…”

Section: Sleep and Its Effect On Oxidative Stressmentioning

confidence: 82%

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

Lopresti

Hood

Drummond

2013

Journal of Affective Disorders

529

412

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Research on major depression has confirmed that it is caused by an array of biopsychosocial and lifestyle factors. Diet, exercise and sleep are three such influences that play a significant mediating role in the development, progression and treatment of this condition. This review summarises animal and human-based studies on the relationship between these three lifestyle factors and major depressive disorder, and their influence on dysregulated pathways associated with depression, namely neurotransmitter processes, immuno-inflammatory pathways, hypothalamic-pituitary-adrenal (HPA) axis disturbances, oxidative stress and antioxidant defence systems, neuroprogression, and mitochondrial disturbances. Increased attention in future clinical studies on the influence of diet, sleep and exercise on major depressive disorder and investigations of their effect on physiological processes will help to expand our understanding and treatment of major depressive disorder. Mental health interventions, taking into account the bidirectional relationship between these lifestyle factors and major depression are also likely to enhance the efficacy of interventions associated with this disorder.

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“…The activated PER and CRY in turn inhibit the activity of the CLOCK/ BMAL complex. In addition to this, recent biochemical and physiological studies have confirmed that sleep deprivation as a strong stressor for the body, increase the level of oxidative stress of the brain, resulting in cognitive dysfunction and memory loss [2].…”

Section: Introductionmentioning

confidence: 92%

Effects of 72 Hours Sleep Deprivation on Liver Circadian Clock Gene Expression and Oxidative Stress in Rats

Tang¹,

Cao²,

Xia³

2017

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Objective: To investigate the effects of 72 hours continuous sleep deprivation (SD) on circadian clock gene expression and oxidative stress in the rat liver. Methods: Twenty healthy male Sprague-Dawley rats were divided into 2 groups (n = 10 each) using a random number table: normal control group (group C), sleep deprivation group (group SD). Group SD was treated with a modified multiple platform water environment method. After 72 hours sleep deprived, the levels of AST (Aspartate transaminase ) and ALT (Alanine aminotransferase) in serum were determined. The contents of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the liver tissue of the rats were examined in both two groups. The expression levels of CLOCK, BMAL1 and CRY1 protein in liver tissue were examined by Western blotting. Results: Compared with group C, the content of MDA, and the levels of AST and ALT in serum were significantly increased (P < 0.05); SOD activity was significantly decreased (P < 0.05); GSH-Px activity was significantly decreased (P < 0.01); and the expression of CLOCK, BMAL1 and CRY1 protein was downregulated in group SD. Conclusion: 72 hours continuous sleep deprivation can downregulate the expression of circadian clock gene and promote oxidative stress in rats.

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Sleep deprivation decreases superoxide dismutase activity in rat hippocampus and brainstem

Cited by 226 publications

References 20 publications

Rapid alterations in cortical protein profiles underlie spontaneous sleep and wake bouts

Rapid alterations in cortical protein profiles underlie spontaneous sleep and wake bouts

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

Effects of 72 Hours Sleep Deprivation on Liver Circadian Clock Gene Expression and Oxidative Stress in Rats

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