| A high glucose condition sensitizes human hepatocytes to hydrogen peroxide-induced cell death. | |
| | |
MedLine Citation:
|
PMID: 21479420 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
|
Oxidative stress is known to play a key role in the progression of liver disease, including non-alcoholic steatohepatitis (NASH), which is often accompanied by hyperglycemia. This study examined the influence of high glucose on oxidative stress-induced hepatic cell death. Hc cells, a normal human hepatocyte-derived cell line, were cultured in normal-to-high glucose (5.5-22 mM)-containing medium with varying concentrations (0.01-1 mM) of hydrogen peroxide. In certain experiments, cyclosporine A (CyA), which inhibits the mitochondrial permeability transition (MPT) pore, or Z-VAD-FMK (z-VAD), a pan-caspase inhibitor, were added to the medium. Cell viability was evaluated using a colorimetric assay. The mode of cell death was determined by nuclear staining methods using Hoechst 33258 and Sytox green. Neither high glucose (22 mM) nor 0.05-0.5 mM of hydrogen peroxide alone killed Hc cells. However, a combination of the two induced cell death, causing the nuclei of Hc cells to become expanded rather than condensed, and the nuclear membrane to become weak. CyA, but not z-VAD, blocked cell death. These results suggest that a high glucose condition may cause human hepatocytes to undergo hydrogen peroxide-induced necrotic cell death. |
| | |
Authors:
|
Hidetaka Shibata; Tatsuki Ichikawa; Kazuhiko Nakao; Hisamitsu Miyaaki; Shigeyuki Takeshita; Motohisa Akiyama; Masumi Fujimoto; Satoshi Miuma; Shougo Kanda; Hironori Yamasaki; Katsumi Eguchi |
Publication Detail:
|
Type: Journal Article |
Journal Detail:
|
Title: Molecular medicine reports Volume: 1 ISSN: 1791-2997 ISO Abbreviation: Mol Med Report Publication Date: 2008 May-Jun |
Date Detail:
|
Created Date: 2011-04-11 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101475259 Medline TA: Mol Med Report Country: Greece |
Other Details:
|
Languages: eng Pagination: 379-85 Citation Subset: - |
Affiliation:
|
The First Department of Internal Medicine, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8501, Japan. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Amplified interleukin-15 expression vectors for cancer immunogene therapy.
Next Document: Analysis of the status of the novel estrogen receptor ? (ER?) coactivator p72 in endometrial cancer ...