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Heme oxygenase-1-mediated partial cytoprotective effect by NO on cadmium-induced cytotoxicity in C6 rat glioma cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Srisook, Klaokwan | - |
dc.contributor.author | Jung, Nam-Hee | - |
dc.contributor.author | Kim, Bum-Rae | - |
dc.contributor.author | Cha, Seok-Ho | - |
dc.contributor.author | Kim, Hye-Sun | - |
dc.contributor.author | Cha, Young-Nam | - |
dc.date.accessioned | 2009-12-31T05:41:38Z | - |
dc.date.available | 2009-12-31T05:41:38Z | - |
dc.date.issued | 2004-12-08 | - |
dc.identifier.citation | Toxicol In Vitro. 2005 Feb;19(1):31-9. | en |
dc.identifier.issn | 0887-2333 (Print) | - |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15582353 | - |
dc.identifier.uri | https://hdl.handle.net/10371/24517 | - |
dc.description.abstract | Heme oxygenase-1 (HO-1) is a 32-kDa stress induced enzyme that degrades heme to carbon monoxide (CO) and biliverdin. By employing RT-PCR and Western blotting techniques, we have examined the HO-1 induction in C6 glioma cells that were treated with cadmium chloride (CdCl(2)) or spermine NONOate (SPER/NO). By employing a cell viability assay, we have also examined the cytoprotective effect of HO-1 induction against the cytotoxicity caused by toxic dose of CdCl(2). In C6 glioma cells exposed to CdCl(2), expression of HO-1 (mRNA and protein) was increased in a dose- and time-dependent manner. Nitric oxide (NO) generated from SPER/NO very rapidly increased HO-1 mRNA expression in the C6 glioma cells. The induction of HO-1 by SPER/NO protected the cells from toxic dose of CdCl(2). The up-regulation of HO-1 mRNA expression by CdCl(2) was inhibited by a pre-incubation of the cells with actinomycin D, a potent inhibitor of mRNA transcription. Upon the inhibition of elevated HO-1 mRNA expression by the use of zinc protoporphyrin IX (ZnPP), an inhibitor of HO activity, the change of HO-1 mRNA expression by ZnPP was not observed. Thus, the glial cell may respond to CdCl(2) toxicity by enhancing the HO-1 expression in its effort to minimize the CdCl(2)-derived oxidative damage, and to survive. In the glioma cells, when the HO-1 expression was elevated by a prior incubation with SPER/NO, the cell viability against the cytotoxicity of CdCl(2) was significantly increased. When the results of our experiment are taken together, we discovered that NO provided a rapid enhancement of HO-1 expression, and it provided a protective effect against CdCl(2)-derived oxidative injury in the C6 rat glioma cells. | en |
dc.language.iso | en | en |
dc.publisher | Elsevier | en |
dc.subject | Animals | en |
dc.subject | Brain Neoplasms/drug therapy/*enzymology/pathology | en |
dc.subject | Cadmium/*toxicity | en |
dc.subject | Cell Line, Tumor | en |
dc.subject | Cell Survival/drug effects | en |
dc.subject | Cytoprotection/*drug effects | en |
dc.subject | Dose-Response Relationship, Drug | en |
dc.subject | Enzyme Induction | en |
dc.subject | Enzyme Inhibitors/pharmacology | en |
dc.subject | Glioma/drug therapy/*enzymology/pathology | en |
dc.subject | Heme Oxygenase (Decyclizing)/antagonists & | en |
dc.subject | inhibitors/*biosynthesis/genetics | en |
dc.subject | Heme Oxygenase-1 | en |
dc.subject | Nitric Oxide/*biosynthesis | en |
dc.subject | Nitric Oxide Donors/pharmacology | en |
dc.subject | Nitrogen Oxides | en |
dc.subject | Protoporphyrins/pharmacology | en |
dc.subject | RNA, Messenger/metabolism | en |
dc.subject | Rats | en |
dc.subject | Reverse Transcriptase Polymerase Chain Reaction | en |
dc.subject | Spermine/*analogs & derivatives/pharmacology | en |
dc.subject | Up-Regulation | en |
dc.title | Heme oxygenase-1-mediated partial cytoprotective effect by NO on cadmium-induced cytotoxicity in C6 rat glioma cells | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 정남희 | - |
dc.contributor.AlternativeAuthor | 김범래 | - |
dc.contributor.AlternativeAuthor | 차석호 | - |
dc.contributor.AlternativeAuthor | 김혜선 | - |
dc.contributor.AlternativeAuthor | 차영남 | - |
dc.identifier.doi | 10.1016/j.tiv.2004.04.012 | - |
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