Akademik Veri Yönetim Sistemi
JOURNAL OF INSECT PHYSIOLOGY, cilt.56, sa.12, ss.1935-1948, 2010 (SCI-Expanded)
The ectoparasitic wasp Nasonia vitripennis produces a proteinaceous venom that induces death in fly hosts by non-paralytic mechanisms Previous in vitro assays have suggested that the primary cause of cell and tissue death is oncosis a non-programmed cell death (PCD) pathway characterized by cellular swelling and lysis However ultrastructural analyses of BTI-TN-5B1 cells exposed to LC(99) doses of wasp venom revealed cellular changes more consistent with apoptosis and/or non-apoptotic PCD than oncosis or necrosis By 3 h after incubation with venom susceptible cells displayed indentations in the nuclear membranes large nucleoli and extensive vacuolization throughout the cytoplasm In the vast majority of venom treated cells annexin V bound to the plasma membrane surface within 15 min after treatment a characteristic consistent with translocation of phosphatidylserine to the cell surface during the early stages of apoptosis Likewise mitochondrial transmembrane potential was depressed in cells within 15 min in venom-treated cells an event that occurred in the absence of mitochondrial swelling or rupturing of cristae Active caspase 3 was detected by fluorescent labeling in nearly all venom treated cells 3 h after exposure to venom and in turn the potent caspase 3 inhibitor Z-VAD-FMK attenuated the morphological changes elicited by wasp venom and afforded protection to BTI-TN-5B1-4 cells (C) 2010 Elsevier Ltd All rights reserved