作者: Adriana Haimovitz-Friedman , Carlos Cordon-Cardo , Alan Alfieri , Maureen McLoughlin , Zvi Fuks
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摘要: Abstract Apoptosis (programmed cell death) serves as a common mechanism of interphase death after radiation exposure in thymic, lymphoid, and hematopoietic cells but has infrequently been documented other adult mammalian types. The present study demonstrates that apoptotic occurs endothelial to clinically relevant doses basic fibroblast growth factor (bFGF) protects against this mode the lethal effects radiation. Radiation produced heterologous double-stranded DNA breaks cells, exhibited similar competence for repair damage presence or absence bFGF. However, subsequent completion process, second process fragmentation became apparent, which was detected only bFGF associated with ladder oligonucleosomal fragments characteristic apoptosis. degradation occurred mainly G0-G1 phase inhibited by stimulation. C3H/HeJ mice exposed whole lung irradiation changes lining pulmonary microvasculature within 6–8 h exposure. given i.v. immediately before development apoptosis these protected pneumonitis. These findings suggest may represent biologically radiation-induced kill nonlymphoid both vitro vivo natural protection mechanisms effect be level resistance normal malignant tissues vivo.