Georg Bauer1. 1. Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, Freiburg, Germany. georg.bauer@uniklinik-freiburg.de
Abstract
PURPOSE: 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.
PURPOSE: 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.
Authors: Arpád Farkas; Werner Hofmann; Imre Balásházy; István Szoke; Balázs G Madas; Mona Moustafa Journal: Radiat Environ Biophys Date: 2011-02-15 Impact factor: 1.925