Low dose radiation and intercellular induction of apoptosis: potential implications for the control of oncogenesis.
OBJECTIVE
This review is focused on the potential impact of low dose radiation effects on intercellular induction of apoptosis and the underlying reactive-oxygen species (ROS)-mediated signaling pathways.


RESULTS
Transformed cells are subject to ROS-mediated apoptosis induction by non-transformed cells ('intercellular induction of apoptosis') and by ROS-mediated autocrine self-destruction. Sensitivity to intercellular induction of apoptosis and autocrine self-destruction are strictly correlated to the expression of the transformed state. Extracellular superoxide anions generated by transformed target cells drive the selectivity and sensitivity of this signaling system which is based on four different signaling pathways. Low dose irradiation of non-transformed cells enhances intercellular induction of apoptosis in transformed cells. This process is controlled by TGF-beta and seems to depend on the induction of peroxidase release. In addition, low dose radiation enhances superoxide anion generation of transformed target cells.


CONCLUSIONS
Low dose radiation-triggered enhancement of intercellular induction of apoptosis and autocrine self-destruction might represent a potential control system during carcinogenesis. It might be the underlying mechanism for the well-known inhibitory effect of low dose radiation on detectable transformation events. However, modifications of the complex intercellular ROS-based signaling system may also lead to configurations in which low dose radiation attenuates ROS-mediated apoptosis induction.
Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, Freiburg, Germany. georg.bauer@uniklinik-freiburg.de
Georg
G
Bauer
D000818:Animals; D017209:Apoptosis / Q000502:physiology / Q000528:radiation effects*; D019898:Autocrine Communication / Q000528:radiation effects; D002471:Cell Transformation, Neoplastic / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D018920:Coculture Techniques; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology* / Q000532:radiotherapy*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000528:radiation effects; D016212:Transforming Growth Factor beta / Q000378:metabolism
D017382:Reactive Oxygen Species; D016212:Transforming Growth Factor beta