Show simple item record

dc.contributor.authorRoudkenar, MH|| Kuwahara, Y|| Baba, T|| Roushandeh, AM|| Ebishima, S|| Abe, S|| Ohkubo, Y|| Fukumoto, M
dc.date.accessioned2018-08-26T08:29:34Z
dc.date.available2018-08-26T08:29:34Z
dc.date.issued2007
dc.identifier10.1269/jrr.06057
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/51809
dc.description.abstractLipocalin 2 (Lcn2, NGAL) is a member of the lipocalin superfamily with diverse functions such as the transport of fatty acids and the induction of apoptosis. Previous reports indicated that expression of Lcn2 is induced under harmful conditions. However, the mechanisms of the induction of Lcn2 expression remain to be elucidated. In this report, we intended to identify the factor or factors that induce Lcn2 expression. Up-regulation of Lcn2 expression after X-ray exposure was detected in the heart, the kidney and especially in the liver. Primary culture of liver component cells revealed that this up-regulation in the liver was induced in hepatocytes. Up-regulation of Lcn2 expression was also detected in HepG2 cells after the administration of X-rays or H2O2. Interestingly, up-regulation of Lcn2 expression after H2O2 treatment was canceled by the addition of the anti-oxidants, dimethylsulfoxide or cysteamine. These results strongly suggest that Lcn2 expression is induced by reactive oxygen species. Therefore, Lcn2 could be a useful biomarker to identify oxidative stress both in vitro and in vivo.
dc.language.isoEnglish
dc.relation.ispartofJOURNAL OF RADIATION RESEARCH
dc.titleOxidative stress induced lipocalin 2 gene expression: Addressing its expression under the harmful conditions
dc.typeArticle
dc.citation.volume48
dc.citation.issue1
dc.citation.spage39
dc.citation.epage44
dc.citation.indexWeb of science
dc.identifier.DOIhttps://doi.org/10.1269/jrr.06057


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record