Programmed cellular response to ionizing radiation damage.
Three forms of radiation response were investigated to evaluate the hypothesis that cellular radiation response is the result of active molecular signaling and not simply a passive physicochemical process. The decision whether or not a cell should respond to radiation-induced damage either by induction of rescue systems, e.g. mobilization of repair proteins, or induction of suicide mechanisms, e.g. programmed cell death, appears to be the expression of intricate cellular biochemistry. A cell must recognize damage in its genetic material and then activate the appropriate responses. Cell type is important; the response of a fibroblast to radiation damage is both quantitatively and qualitatively different from that of a lymphocyte. The programmed component of radiation response is significant in radiation oncology and predicted to create unique opportunities for enhanced treatment success.
Crompton
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Department of Radiation Medicine, Paul Scherrer Institute, Villigen-PSI, Switzerland. crompton@psi.ch
D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D002110:Caffeine / Q000494:pharmacology; D002453:Cell Cycle / Q000528:radiation effects; D002478:Cells, Cultured; D006224:Cricetinae; D003412:Cricetulus; D004247:DNA / Q000378:metabolism / Q000528:radiation effects; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000528:radiation effects; D008297:Male; D051379:Mice; D011838:Radiation-Sensitizing Agents / Q000494:pharmacology; D019311:Staurosporine / Q000494:pharmacology
D011838:Radiation-Sensitizing Agents; D002110:Caffeine; D004247:DNA; D019311:Staurosporine