Abstract
SPECIFIC AIMSMany studies have demonstrated that 1-β-D-arabinofuranosylcytosine (Ara-C) triggers a wide spectrum of intracellular signals, which may contribute downstream of drug-DNA incorporation to modulate Ara-C cytotoxicity. Therefore, in this study we sought to determine the respective roles of reactive oxygen species (ROS) and p53/p56 Lyn kinase in the regulation of sphingomyelinase (SMase) activation in Ara-C-triggered JNK activation and apoptosis in leukemic myeloid cells.PRINCIPAL FINDINGSU937 and HL-60 cells were treated in kinetic experiments with 40 μM Ara-C and analyzed for cell viability and DNA fragmentation using the [3H]thymidine release assay, poly (ADP-ribose) polymerase (PARP) cleavage, and DAPI staining. Ara-C induced a significant loss of cell viability with DNA fragmentation of 9.7% as soon as 6 h and 45.9% at 24 h. We also observed typical morphological features of apoptosis by DAPI staining and PARP cleavage. The enumeration of morphologically apoptotic cells was estimated at 31% ...
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
