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Heme oxygenase-1-mediated partial cytoprotective effect by NO on cadmium-induced cytotoxicity in C6 rat glioma cells

Cited 27 time in Web of Science Cited 25 time in Scopus
Authors
Srisook, Klaokwan; Jung, Nam-Hee; Kim, Bum-Rae; Cha, Seok-Ho; Kim, Hye-Sun; Cha, Young-Nam
Issue Date
2004-12-08
Publisher
Elsevier
Citation
Toxicol In Vitro. 2005 Feb;19(1):31-9.
Keywords
AnimalsBrain Neoplasms/drug therapy/*enzymology/pathologyCadmium/*toxicityCell Line, TumorCell Survival/drug effectsCytoprotection/*drug effectsDose-Response Relationship, DrugEnzyme InductionEnzyme Inhibitors/pharmacologyGlioma/drug therapy/*enzymology/pathologyHeme Oxygenase (Decyclizing)/antagonists &inhibitors/*biosynthesis/geneticsHeme Oxygenase-1Nitric Oxide/*biosynthesisNitric Oxide Donors/pharmacologyNitrogen OxidesProtoporphyrins/pharmacologyRNA, Messenger/metabolismRatsReverse Transcriptase Polymerase Chain ReactionSpermine/*analogs & derivatives/pharmacologyUp-Regulation
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.
ISSN
0887-2333 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15582353

http://hdl.handle.net/10371/24517
DOI
https://doi.org/10.1016/j.tiv.2004.04.012
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College of Medicine/School of Medicine (의과대학/대학원)Pharmacology (약리학전공)Journal Papers (저널논문_약리학전공)
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