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Article: Rapid induction of apoptosis in human keratinocytes with the photosensitizer QLT0074 via a direct mitochondrial action

TitleRapid induction of apoptosis in human keratinocytes with the photosensitizer QLT0074 via a direct mitochondrial action
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2003
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1360-8185
Citation
Apoptosis, 2003, v. 8 n. 3, p. 269-275 How to Cite?
AbstractQLT0074 is a newly introduced, porphyrin-derivative for use in photodynamic therapy (PDT). In the current study, the intracellular distribution of QLT0074 and the mode of cell death induced by photosensitization with this compound in vitro were assessed for transformed human HaCaT keratinocytes. Fluorescence microscopy studies indicated a distribution of the drug to the cytoplasm, nuclear membrane and mitochondria of these cells. In the absence of light, QLT0074 produced no evidence of apoptosis-related biochemical changes or affected cell viability. When combined with blue light exposure, cytotoxicity was exerted in a QLT0074- and light-dose-related manner. Appearance of the mitochondrial protein cytochrome c in the cytosolic fraction and expression of the apoptosis-associated mitochondrial 7A6 antigen were demonstrable following photosensitization at nanomolar levels of QLT0074. Evidence of processing of the apoptosis-effector molecules caspase-3, -6, -7, -8 and -9 as well as cleavage of the caspase-3 substrate poly (ADP-ribose) polymerase (PARP) were demonstrable subsequent to cytochrome c release after PDT. Treatment with the anti-oxidant pyrrolidine dithiocarbamate (PDTC) inhibited cytochrome c release, caspase-3 activation and PARP cleavage associated with PDT thereby supporting the contention that QLT0074 induces apoptosis through the generation of reactive oxygen species upon light activation. QLT0074 is a potent photosensitizer with the capacity to directly initiate apoptosis by acting upon mitochondria.
Persistent Identifierhttp://hdl.handle.net/10722/91685
ISSN
2015 Impact Factor: 3.592
2015 SCImago Journal Rankings: 1.554
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Ren_HK
dc.contributor.authorBounds, DJen_HK
dc.contributor.authorGranville, Den_HK
dc.contributor.authorIp, SHen_HK
dc.contributor.authorJiang, Hen_HK
dc.contributor.authorMargaron, Pen_HK
dc.contributor.authorHunt, DWCen_HK
dc.date.accessioned2010-09-17T10:23:19Z-
dc.date.available2010-09-17T10:23:19Z-
dc.date.issued2003en_HK
dc.identifier.citationApoptosis, 2003, v. 8 n. 3, p. 269-275en_HK
dc.identifier.issn1360-8185en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91685-
dc.description.abstractQLT0074 is a newly introduced, porphyrin-derivative for use in photodynamic therapy (PDT). In the current study, the intracellular distribution of QLT0074 and the mode of cell death induced by photosensitization with this compound in vitro were assessed for transformed human HaCaT keratinocytes. Fluorescence microscopy studies indicated a distribution of the drug to the cytoplasm, nuclear membrane and mitochondria of these cells. In the absence of light, QLT0074 produced no evidence of apoptosis-related biochemical changes or affected cell viability. When combined with blue light exposure, cytotoxicity was exerted in a QLT0074- and light-dose-related manner. Appearance of the mitochondrial protein cytochrome c in the cytosolic fraction and expression of the apoptosis-associated mitochondrial 7A6 antigen were demonstrable following photosensitization at nanomolar levels of QLT0074. Evidence of processing of the apoptosis-effector molecules caspase-3, -6, -7, -8 and -9 as well as cleavage of the caspase-3 substrate poly (ADP-ribose) polymerase (PARP) were demonstrable subsequent to cytochrome c release after PDT. Treatment with the anti-oxidant pyrrolidine dithiocarbamate (PDTC) inhibited cytochrome c release, caspase-3 activation and PARP cleavage associated with PDT thereby supporting the contention that QLT0074 induces apoptosis through the generation of reactive oxygen species upon light activation. QLT0074 is a potent photosensitizer with the capacity to directly initiate apoptosis by acting upon mitochondria.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=1360-8185en_HK
dc.relation.ispartofApoptosisen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleRapid induction of apoptosis in human keratinocytes with the photosensitizer QLT0074 via a direct mitochondrial actionen_HK
dc.typeArticleen_HK
dc.identifier.emailLi, RA:ronaldli@HKUCC.hku.hken_HK
dc.identifier.authorityLi, RA=rp1352en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1023/A:1023624922787en_HK
dc.identifier.pmid12766487-
dc.identifier.scopuseid_2-s2.0-0037898884en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037898884&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.issue3en_HK
dc.identifier.spage269en_HK
dc.identifier.epage275en_HK
dc.identifier.isiWOS:000182721900006-

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