Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-3-30
pubmed:abstractText
One of the characteristics of hepatitis C virus (HCV) infection is the unusual augmentation of oxidative stress, which is exacerbated by iron accumulation in the liver, as observed frequently in hepatitis C patients. Using a transgenic mouse model, the core protein of HCV was shown previously to induce the overproduction of reactive oxygen species (ROS) in the liver. In the present study, the impact of iron overloading on the oxidant/antioxidant system was examined using this mouse model and cultured cells. Iron overloading caused the induction of ROS as well as antioxidants. However, the augmentation of some antioxidants, including heme oxygenase-1 and NADH dehydrogenase, quinone 1, was compromised by the presence of the core protein. The attenuation of iron-induced augmentation of heme oxygenase-1 was also confirmed in HepG2 cells expressing the core protein. This attenuation was not dependent on the Nrf2 transcription factor. Thus, HCV infection not only induces oxidative stress but also hampers the iron-induced antioxidant activation in the liver, thereby exacerbating oxidative stress that would facilitate hepatocarcinogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1096-9071
pubmed:author
pubmed:copyrightInfo
(c) 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
776-92
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Hepatitis C virus core protein compromises iron-induced activation of antioxidants in mice and HepG2 cells.
pubmed:affiliation
Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't