Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/62009
DC FieldValueLanguage
dc.contributor.authorYang, N.C.en_US
dc.contributor.author胡淼琳zh_TW
dc.contributor.authorJeng, K.C.G.en_US
dc.contributor.authorHo, W.M.en_US
dc.contributor.authorHu, M.L.en_US
dc.date2002zh_TW
dc.date.accessioned2014-06-09T06:26:14Z-
dc.date.available2014-06-09T06:26:14Z-
dc.identifier.issn0024-3205zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/62009-
dc.description.abstractDehydroepiandrosterone (DHEA), a major steroid secreted by the adrenal gland, is known to have antiproliferative effects but the mechanism is unclear. We recently reported that DHEA induces growth inhibition and apoptosis in BV-2 cells and these effects are inversely associated with glucose concentrations in the medium. Here, we further showed that incubation of BV-2 cells with DHEA under glucose deprivation (GO) led to dose- and time-dependent decrease in cellular ATP levels. The decrease in ATP preceded growth inhibition and apoptosis induced by DHEA and all these effects of DHEA (i.e., loss of ATP, antiproliferation and apoptosis) were prevented by glucose added at 4.5 mg/ml (G4.5) during incubation. In addition, two ATP-depleting agents, iodoacetic acid (IAA) and 2,4-dinitrophenylhydrazine (2,4-DNP), potentiated the antiproliferative and apoptotic effects of DHEA. We also determined whether decrease in nucleic acid synthesis (due to glucose-6-phosphate dehydrogenase inhibition by DHEA) contributes to DHEA-induced antiproliferation and apoptosis. Using a mixture of deoxyribonucleotides (DN) and ribonucleotides (RN), we showed that DNRN had little or no effect on DHEA-induced growth inhibition and apoptosis. We also showed that mevalonic acid (MVA) did not affect DHEA-induced antiproliferation and apoptotic effects, indicating that protein isoprenylation and membrane association are not affected by DHEA in BV-2 cells. Taken together, the present results demonstrate that depletion of ATP by DHEA plays an important role in DHEA-induced antiproliferation and apoptosis of BV-2 cells. (C) 2002 Elsevier Science Inc. All rights reserved.en_US
dc.language.isoen_USzh_TW
dc.relationLife Sciencesen_US
dc.relation.ispartofseriesLife Sciences, Volume 70, Issue 17, Page(s) 1979-1988.en_US
dc.relation.urihttp://dx.doi.org/10.1016/s0024-3205(01)01542-9en_US
dc.subjectDHEAen_US
dc.subjectantproliferationen_US
dc.subjectapoptosisen_US
dc.subjectATP depletionen_US
dc.subjectcolonic adenocarcinoma cellsen_US
dc.subjectdehydroepiandrosterone-sulfateen_US
dc.subjectoxidativeen_US
dc.subjectstressen_US
dc.subjectcycle arresten_US
dc.subjectglucose-6-phosphate-dehydrogenaseen_US
dc.subjectratsen_US
dc.subjectproliferationen_US
dc.subjectsteroidsen_US
dc.subject2',7'-dichlorofluorescinen_US
dc.subjecthepatocytesen_US
dc.titleATP depletion is an important factor in DHEA-induced growth inhibition and apoptosis in BV-2 cellsen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/s0024-3205(01)01542-9zh_TW
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en_US-
item.fulltextno fulltext-
item.grantfulltextnone-
item.openairetypeJournal Article-
Appears in Collections:食品暨應用生物科技學系
Show simple item record
 

Google ScholarTM

Check

Altmetric

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.