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

English | 正體中文 | 简体中文 | 全文筆數/總筆數 : 45172/58348 (77%)
造訪人次 : 2465783 線上人數 : 167

RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.

Taipei Medical University Institutional Repository > 醫學院 > 醫學系 > 生物化學暨細胞分子生物學科 > 期刊論文 > Item 987654321/3054

請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/3054

題名:	Sleep deprivation predisposes liver to oxidative stress and phospholipid damage: a quantitative molecular imaging study
作者:	麥富德 Chang HM;Mai FD;Chen BJ;Huang YL;Lan CT;Ling YC
貢獻者:	醫學系生化學科
日期:	2008
上傳時間:	2009-08-21 16:34:24 (UTC+8)
摘要:	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 micromol g-1 to 9.4 micromol 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
關聯:	J. Anat.(212):295-305.
資料類型:	article
顯示於類別:	[生物化學暨細胞分子生物學科] 期刊論文

文件中的檔案:

檔案	大小	格式	瀏覽次數
121.pdf	1647Kb	Adobe PDF	90	檢視/開啟
全文.txt	0Kb	Text	289	檢視/開啟
摘要.pdf	38Kb	Adobe PDF	62	檢視/開啟

在TMUIR中所有的資料項目都受到原著作權保護.

TAIR相關文章

著作權聲明 Copyright Notice

本平台之數位內容為臺北醫學大學所收錄之機構典藏，包含體系內各式學術著作及學術產出。秉持開放取用的精神，提供使用者進行資料檢索、下載與取用，惟仍請適度、合理地於合法範圍內使用本平台之內容，以尊重著作權人之權益。商業上之利用，請先取得著作權人之授權。
The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.
瀏覽或使用本平台，視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例，並不得為任何不法目的使用TMUIR。
By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.
本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者，煩請權利人通知本平台維護人員([email protected])，將立即採取移除該數位著作等補救措施。
TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

資料載入中.....