scholarly journals Intercellular and Intracellular Signaling Pathways Mediating Ionizing Radiation-Induced Bystander Effects

2007 ◽  
Vol 48 (2) ◽  
pp. 87-95 ◽  
Author(s):  
Nobuyuki HAMADA ◽  
Hideki MATSUMOTO ◽  
Takamitsu HARA ◽  
Yasuhiko KOBAYASHI
Keyword(s):  
Ionizing Radiation ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Bystander Effects ◽  
Intracellular Signaling Pathways ◽  
Radiation Induced

Signaling Pathways Underpinning the Manifestations of Ionizing Radiation-Induced Bystander Effects

2011 ◽  
Vol 4 (2) ◽  
pp. 79-95 ◽  
Author(s):  
Nobuyuki Hamada ◽  
Munetoshi Maeda ◽  
Kensuke Otsuka ◽  
Masanori Tomita
Keyword(s):  
Ionizing Radiation ◽  
Signaling Pathways ◽  
Bystander Effects ◽  
Radiation Induced

scholarly journals Interaction of dual intracellular signaling pathways activated by the melanocortin-3 receptor.

1994 ◽  
Vol 269 (18) ◽  
pp. 13162-13166
Author(s):  
Y. Konda ◽  
I. Gantz ◽  
J. DelValle ◽  
Y. Shimoto ◽  
H. Miwa ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Intracellular Signaling Pathways

Commentary on radiation-induced bystander effects

2004 ◽  
Vol 23 (2) ◽  
pp. 91-94 ◽  
Author(s):  
Eric G Wright
Keyword(s):  
Free Radical ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Inflammatory Responses ◽  
Genetic Alterations ◽  
Bystander Effects ◽  
Intercellular Signalling ◽  
Radiation Induced ◽  
Radical Generation ◽  
In Cells

The paradigm of genetic alterations being restricted to direct DNA damage after exposure to ionizing radiation has been challenged by observations in which effects of ionizing radiation arise in cells that in themselves receive no radiation exposure. These effects are demonstrated in cells that are the descendants of irradiated cells (radiation-induced genomic instability) or in cells that are in contact with irradiated cells or receive certain signals from irradiated cells (radiation-induced bystander effects). Bystander signals may be transmitted either by direct intercellular communication through gap junctions, or by diffusible factors, such as cytokines released from irradiated cells. In both phenomena, the untargeted effects of ionizing radiation appear to be associated with free radical-mediated processes. There is evidence that radiation-induced genomic instability may be a consequence of, and in some cell systems may also produce, bystander interactions involving intercellular signalling, production of cytokines and free radical generation. These processes are also features of inflammatory responses that are known to have the potential for both bystander-mediated and persisting damage as well as for conferring a predisposition to malignancy. Thus, radiation-induced genomic instability and untargeted bystander effects may reflect interrelated aspects of inflammatory type responses to radiation-induced stress and injury and contribute to the variety of the pathological consequences of radiation exposures.

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