Low dose radiation and intercellular induction of apoptosis: potential implications for the control of oncogenesis

• Published in: International journal of radiation biology Vol. 83; no. 11-12; pp. 873 - 888
• Main Author: Bauer, Georg
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.01.2007; Taylor & Francis
• Subjects: Animals; apoptosis; Apoptosis - physiology; Apoptosis - radiation effects; Autocrine Communication - radiation effects; Cell Transformation, Neoplastic - metabolism; Cell Transformation, Neoplastic - pathology; Cell Transformation, Neoplastic - radiation effects; Coculture Techniques; Humans; Low dose radiation; Models, Biological; Neoplasms - metabolism; Neoplasms - pathology; Neoplasms - radiotherapy; reactive oxygen; Reactive Oxygen Species - metabolism; Signal Transduction - radiation effects; Transforming Growth Factor beta - metabolism
• ISSN: 0955-3002; 1362-3095
• DOI: 10.1080/09553000701727523

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 selfdestruction 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.