ID 110651
Author
Lu, Guangming Second Department of Internal Medicine, The University of Tokushima School of Medicine
Shimizu, Ichiro Second Department of Internal Medicine, The University of Tokushima School of Medicine
Cui, Xuezhi Second Department of Internal Medicine, The University of Tokushima School of Medicine
Itonaga, Mina Second Department of Internal Medicine, The University of Tokushima School of Medicine
Tamaki, Katsuyoshi Second Department of Internal Medicine, The University of Tokushima School of Medicine
Fukuno, Hiroshi Second Department of Internal Medicine, The University of Tokushima School of Medicine
Inoue, Hiroshi Second Department of Internal Medicine, The University of Tokushima School of Medicine
Honda, Hirohito Second Department of Internal Medicine, The University of Tokushima School of Medicine
Ito, Susumu Second Department of Internal Medicine, The University of Tokushima School of Medicine Tokushima University Educator and Researcher Directory
Keywords
interferon-α
oxidative stress
lipid peroxidation
hepatic fibrosis
hepatic stellate cell
antioxidant enzyme
Content Type
Journal Article
Description
Oxidative stress has been implicated as a cause of hepatic fibrosis, and hepatic stellate cells (HSCs), which are the most important collagen-producing cell types, have been reported to be activated by lipid peroxidation products. Antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) provide a defense system that plays a critical role in protecting the cell from free radical damage, particularly lipid peroxidation. To elucidate the antioxidant activity of interferon-α (IFN-α), the effects of IFN-α on rat hepatocytes undergoing oxidative stress and HSCs in primary culture as well as isolated rat liver mitochondria were examined. IFN-α was observed to dose-dependently increase the immunoreactive protein levels of copper, zinc-and manganese-dependent SOD as well as the enzyme activities of GPx, and decrease the lipid peroxidation product levels and oxidative burst both in stressed hepatocytes and activated HSCs GPx activities, however, were not detected in the latter cells. IFN-α also inhibited HSC activation and lipid peroxidation in liver mitochondria. These findings suggest that IFN-α may enhance biological defense activities against oxidative stress and function as a potent fibrosuppressant by protecting hepatocytes and hepatic stellate cells from lipid peroxidation in vivo.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
49
Issue
3-4
Start Page
172
End Page
181
Sort Key
172
Published Date
2002
EDB ID
FullText File
language
eng
TextVersion
Publisher
departments
Medical Sciences