Sleep deprivation predisposes liver to oxidative stress and phospholipid damage: A quantitative molecular imaging study

Hung Ming Chang, Fu Der Mai, Bo Jung Chen, Un In Wu, Yi Lun Huang, Chyn Tair Lan, Yong Chien Ling

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Sleep disorders are associated with an increased rate of various metabolic disturbances, which may be related to oxidative stress and consequent lipid peroxidation. Since hepatic phosphatidylcholine plays an important role in metabolic regulation, the aim of the present study was to determine phosphatidylcholine expression in the liver following total sleep deprivation. To determine the effects of total sleep deprivation, we used adult rats implanted for polygraphic recording. Phosphatidylcholine expression was examined molecularly by the use of time-of-flight secondary ion mass spectrometry, along with biochemical solid-phase extraction. The parameters of oxidative stress were investigated by evaluating the hepatic malondialdehyde levels as well as heat shock protein 25 immunoblotting and immunohistochemistry. In normal rats, the time-of-flight secondary ion mass spectrometry spectra revealed specific peaks (m/z 184 and 224) that could be identified as molecular ions for phosphatidylcholine. However, following total sleep deprivation, the signals for phosphatidylcholine were significantly reduced to nearly one-third of the normal values. The results of solid-phase extraction also revealed that the phosphatidylcholine concentration was noticeably decreased, from 15.7 μmol.g-1 to 9.4 μmol.g-1, after total sleep deprivation. By contrast, the biomarkers for oxidative stress were drastically up-regulated in the total sleep deprivation-treated rats as compared with the normal ones (4.03 vs. 1.58 nmol.mg-1 for malondialdehyde levels, and 17.1 vs. 6.7 as well as 1.8 vs. 0.7 for heat shock protein 25 immunoblotting and immunoreactivity, respectively). Given that phosphatidylcholine is the most prominent component of all plasma lipoproteins, decreased expression of hepatic phosphatidylcholine following total sleep deprivation may be attributed to the enhanced oxidative stress and the subsequent lipid peroxidation, which would play an important role in the formation or progression of total sleep deprivation-induced metabolic diseases.

Original languageEnglish
Pages (from-to)295-305
Number of pages11
JournalJournal of Anatomy
Volume212
Issue number3
DOIs
Publication statusPublished - Mar 2008

Fingerprint

Molecular Imaging
Sleep Deprivation
sleep
phospholipid
Phosphatidylcholines
phosphatidylcholines
Phospholipids
phospholipids
Oxidative Stress
oxidative stress
image analysis
liver
damage
Liver
Secondary Ion Mass Spectrometry
heat shock
Solid Phase Extraction
ions
solid phase extraction
Heat-Shock Proteins

Keywords

  • Hepatic injury
  • Lipid peroxidation
  • Metabolic dysfunction
  • Molecular image
  • Quantitative image analysis
  • Sleep disorder

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Anatomy

Cite this

Sleep deprivation predisposes liver to oxidative stress and phospholipid damage : A quantitative molecular imaging study. / Chang, Hung Ming; Mai, Fu Der; Chen, Bo Jung; Wu, Un In; Huang, Yi Lun; Lan, Chyn Tair; Ling, Yong Chien.

In: Journal of Anatomy, Vol. 212, No. 3, 03.2008, p. 295-305.

Research output: Contribution to journalArticle

Chang, Hung Ming ; Mai, Fu Der ; Chen, Bo Jung ; Wu, Un In ; Huang, Yi Lun ; Lan, Chyn Tair ; Ling, Yong Chien. / Sleep deprivation predisposes liver to oxidative stress and phospholipid damage : A quantitative molecular imaging study. In: Journal of Anatomy. 2008 ; Vol. 212, No. 3. pp. 295-305.
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