DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park, EK | ko |
dc.contributor.author | Kwon, KB | ko |
dc.contributor.author | Park, KI | ko |
dc.contributor.author | Park, BH | ko |
dc.contributor.author | Jhee, EC | ko |
dc.date.accessioned | 2024-03-22T03:01:55Z | - |
dc.date.available | 2024-03-22T03:01:55Z | - |
dc.date.created | 2024-03-21 | - |
dc.date.created | 2024-03-21 | - |
dc.date.issued | 2002-07 | - |
dc.identifier.citation | EXPERIMENTAL AND MOLECULAR MEDICINE, v.34, no.3, pp.250 - 257 | - |
dc.identifier.issn | 1226-3613 | - |
dc.identifier.uri | http://hdl.handle.net/10203/318675 | - |
dc.description.abstract | Diallyl disulfide (DADS) induced apoptosis through the caspase-3 dependent pathway in leukemia cells was earlier reported from this laboratory. In this study, we investigated the involvement of Ca2+ in DADS-induced apoptotic cell death of HCT-15, human colon cancer cell line. DADS induced the elevation of cytosolic Ca2+ by biphasic pattern; rapid Ca2+ peak at 3 min and following slow and sustained elevation till 3 h after the addition of DADS. Production of H2O2 was also observed with its peak value at 4 h. Apoptotic pathways including the sequence of caspase-3 activation, poly(ADP-ribose) polymerase cleavage, and DNA fragmentation by DADS were completely blocked by various inhibitors such as specific caspase-3 inhibitor, free radical scavenger, and intracellular Ca2+ chelator. N-acetylcystein and catalase treatment prevented the accumulation of H2O2 and later caspase-3 dependent apoptotic pathway. However, these radical scavengers did not block the elevation of intracellular Ca2+. Treatment of cells with 1,2-bis(2-aminophenoxyethane)-N,N,N-tetraacetic acid tetralkis -acetoxymethylester (BAPTA-AM), cellular Ca2+ chelator, resulted in a complete blockage of the caspase-3 dependent apoptotic pathway of HCT-15 cells. It abolished the elevation of intracellular Ca2+, and furthermore, completely inhibited the production of H2O2. These results indicate that cytosolic Ca2+ elevation is an earlier signaling event in apoptosis of HCT-15 cells. Collectively, our data demonstrate that DADS can induce apoptosis in HCT-15 cells through the sequential mechanism of Ca2+ homeostasis disruption, accumulation of H2O2, and resulting caspase-3 activation. | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Role of Ca2+ in diallyl disulfide-induced apoptotic cell death of HCT-15 cells | - |
dc.type | Article | - |
dc.identifier.wosid | 000177710300010 | - |
dc.identifier.scopusid | 2-s2.0-0037205963 | - |
dc.type.rims | ART | - |
dc.citation.volume | 34 | - |
dc.citation.issue | 3 | - |
dc.citation.beginningpage | 250 | - |
dc.citation.endingpage | 257 | - |
dc.citation.publicationname | EXPERIMENTAL AND MOLECULAR MEDICINE | - |
dc.identifier.doi | 10.1038/emm.2002.35 | - |
dc.contributor.localauthor | Park, BH | - |
dc.contributor.nonIdAuthor | Park, EK | - |
dc.contributor.nonIdAuthor | Kwon, KB | - |
dc.contributor.nonIdAuthor | Park, KI | - |
dc.contributor.nonIdAuthor | Jhee, EC | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | diallyl disulfide | - |
dc.subject.keywordAuthor | Ca2+ | - |
dc.subject.keywordAuthor | H2O2 | - |
dc.subject.keywordAuthor | caspase-3 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | HCT-15 cells | - |
dc.subject.keywordPlus | DNA-DEGRADATION | - |
dc.subject.keywordPlus | CALCIUM | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CLEAVAGE | - |
dc.subject.keywordPlus | CASPASE-3 | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | MITOCHONDRIA | - |
dc.subject.keywordPlus | MECHANISM | - |
dc.subject.keywordPlus | IONOPHORE | - |
dc.subject.keywordPlus | RADICALS | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.