Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells [1999];_WJD_2016-0913_V001R01_IR92_
Source (資訊來源):
http://www.sciencedirect.com/science/article/pii/S0003986198910670
Info cited on 2016-09-13-WD2 (資訊引用於 中華民國105年9月13日) by 湯偉晉 (WeiJin Tang)
Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells [1999];_WJD_2016-0913_V001R01_IR92_
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2016-09-13
Archives of Biochemistry and Biophysics
Volume 363, Issue 1, 1 March 1999, Pages 33-42
Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells
Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells
Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells
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Yoshihiro Higuchi a, 1, Shigeru Matsukawa b
a Department of Pharmacology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan
b The Central Research Laboratories, Fukui Medical School, Matsuoka, Fukui, 910-1193, Japan
Received 29 June 1998, Revised 30 November 1998, Available online 6 April 2002
doi:10.1006/abbi.1998.1067
Abstract
Glutathione (GSH) depletion caused byl-buthionine-(S,R)-sulfoximine (BSO) induced apoptosis that was recognized by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick endo-labeling (TUNEL), nuclear DNA staining with fluorescence dye, and internucleosomal DNA fragmentation in C6 rat glioma cells. The BSO-induced cell death was associated with caspase-3 activation. Lipid peroxidation and protein kinase C (PK-C) activation were observed during the apoptosis of C6 cells, and these events were inhibited by antioxidants and iron chelators without affecting BSO-induced GSH depletion. Furthermore, approximately 2 Mbp giant DNA fragments were observed in the BSO-treated cells. The giant DNA fragmentation were followed by approximately 30–700 kbp and then less than 100 kbp, including internucleosomal DNA fragmentations. Such serial DNA degradation was prevented by the antioxidants, the iron chelators, and the PK-C inhibitors. These results suggest that during apoptosis induced by GSH-depletion caused by BSO, reactive oxygen species endogenously produced cause lipid peroxidation and that the lipid peroxidation induced PK-C activation, processes which are thought to be involved in the giant DNA, high-molecular-weight DNA, and the internucleosomal DNA fragmentations.
Keywords
apoptosis; reactive oxygen species (ROS); giant DNA fragments; glutathione; lipid peroxidation; protein kinase C
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Davies, K. T. A.
1
To whom correspondence should be addressed at Department of Pharmacology, Kanazawa University School of Medicine, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8640, Japan. Fax: +81-76-234-4227. E-mail:higuchi@kenroku.kanazawa-u.ac.jp.
Copyright © 1999 Academic Press. All rights reserved.
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