CERAMIDE PERMEABILIZATION OF MITOCHONDRIAL OUTER MEMBRANE: PHARMACOLOGICAL CHARACTERIZATION AND RELATION TO MAC AND BAX

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dc.contributor.advisorColombini, Marcoen_US
dc.contributor.authorHudak, Suzanne Jen_US
dc.contributor.departmentBiochemistryen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.date.accessioned2006-02-04T07:50:34Z
dc.date.available2006-02-04T07:50:34Z
dc.date.issued2005-12-08en_US
dc.description.abstractIn apoptosis, the mitochondrial outer membrane (MOM) becomes permeable, releasing proteins. This permeability has been attributed to the action of various factors, including mitochondrial apoptosis-induced channel (MAC), Bax and ceramide channels. Amphiphilic cations that inhibited MAC and Bax-induced permeabilization were tested on ceramide-induced permeabilization of MOM of mammalian and yeast mitochondria, as well as liposomes. Both propranolol and dibucaine inhibited C2- and C16-ceramide-induced permeabilization of mammalian MOM with an IC50 for C16-ceramide of 410 and 230 M, respectively. In yeast mitochondria, propranolol and dibucaine inhibited C2-ceramide-induced permeabilization, but potentiated the effect of C16-ceramide. Similar results were obtained in liposome experiments. These results suggest that inhibition is via another factor found in mammalian cells but not the other systems. The pharmacology of ceramide membrane permeabilization is inconsistent with that of MAC but is compatible to that of Bax.en_US
dc.format.extent4574084 bytes
dc.format.mimetypeapplication/pdf
dc.identifier.urihttp://hdl.handle.net/1903/3240
dc.language.isoen_US
dc.subject.pqcontrolledBiophysics, Generalen_US
dc.titleCERAMIDE PERMEABILIZATION OF MITOCHONDRIAL OUTER MEMBRANE: PHARMACOLOGICAL CHARACTERIZATION AND RELATION TO MAC AND BAXen_US
dc.typeThesisen_US

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