Skip Navigation



Carcinogenesis Advance Access published online on September 8, 2005
Carcinogenesis, doi:10.1093/carcin/bgi224
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
27/2/245    most recent
bgi224v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Hu, B.
Right arrow Articles by Yu, Z.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hu, B.
Right arrow Articles by Yu, Z.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received June 9, 2005
Revised August 26, 2005
Accepted September 3, 2005

CANCER BIOLOGY

The time and spatial effects of bystander response in mammalian cells induced by low dose radiation

Burong Hu 1, Lijun Wu 1*, Wei Han 1, Leilei Zhang 1, shaopeng Chen 1, An Xu 1, Tom K. Hei 2, and Zengliang Yu 1

1 Key Laboratory of Ion Beam Bioengineering, Institute of Plasma Physics, Chinese Academy of Sciences, Hefei 230031, People's Republic of China
2 Center for Radiological Research, College of Physicians and Surgeons,Columbia University, New York 10032, USA

* To whom correspondence should be addressed.
Lijun Wu, E-mail: ljw{at}ipp.ac.cn


  Abstract

Bystander effects induced by low dose of ionizing radiation have been shown to be widely existed in many cell types and may have a significant impact on radiation risk assessment. Though many studies have been reported on this phenomenological observation, the mechanisms underlying this process are not clear, especially on the questions of how soon after irradiation the bystander effects can be initiated and how far this bystander signal can be propagated once it started. DNA double-strand breaks (DSBs) induced by ionizing radiation or carcinogenic chemicals can be visualized in situ using {gamma}-H2AX immunofluorescent staining. Our previous studies have shown that in situ visualization of DSBs could be used to assess irradiation-induced extranuclear/extracellular (bystander) effect at an early stage after irradiation. In the present studies, we used this method to investigate the time and spatial effects of damage signals to un-irradiated bystander cells. The results showed that increased DSBs in irradiated and unirradiated bystander areas could be visualized 2min after radiation and reached its maximum 30min after radiation. The average levels of DSBs formation at 30 minutes post 1cGy irradiation in the irradiated and unirradiated bystander areas were 3 and 2 folds higher than those of the sham-irradiated control cells, respectively. Afterwards, the formation of DSBs declined with incubation time and maintained steady for at least 6 hrs at a level which was statistically higher than their controls. The results also showed that the bystander signal derived from irradiated cells could be transferred to anywhere in the dish and the percentage of DSBs in the cells in unirradiated bystander cells was not dependent on the dose delivered. Moreover, the fraction of DSBs positive cells in unirradiated bystander areas showed a time dependent increases based on its distance to irradiated area at very early stage post irradiation. Both lindane and DMSO significantly suppressed the yield of DSBs in the cells of unirradiated bystander areas, which suggest that gap junctional intercellular communication (GJIC) and reactive oxygen species (ROS) played important roles in the induction of the bystander effects both in irradiated and unirradiated bystander areas.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
J. S. Dickey, B. J. Baird, C. E. Redon, M. V. Sokolov, O. A. Sedelnikova, and W. M. Bonner
Intercellular communication of cellular stress monitored by {gamma}-H2AX induction
Carcinogenesis, October 1, 2009; 30(10): 1686 - 1695.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
S. Burdak-Rothkamm, K. Rothkamm, and K. M. Prise
ATM Acts Downstream of ATR in the DNA Damage Response Signaling of Bystander Cells
Cancer Res., September 1, 2008; 68(17): 7059 - 7065.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
M. Mancuso, E. Pasquali, S. Leonardi, M. Tanori, S. Rebessi, V. Di Majo, S. Pazzaglia, M. P. Toni, M. Pimpinella, V. Covelli, et al.
From the Cover: Oncogenic bystander radiation effects in Patched heterozygous mouse cerebellum
PNAS, August 26, 2008; 105(34): 12445 - 12450.
[Abstract] [Full Text] [PDF]

Home page
 Radiat Prot DosimetryHome page
L. B. Smilenov, E. J. Hall, W. M. Bonner, and O. A. Sedelnikova
A microbeam study of DNA double-strand breaks in bystander primary human fibroblasts
Radiat Prot Dosimetry, December 1, 2006; 122(1-4): 256 - 259.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.