Oxidative metabolism, gap junctions and the ionizing radiation-induced bystander effect

被引:254
作者
Azzam, EI
de Toledo, SM
Little, JB
机构
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Radiol, Newark, NJ 07103 USA
[2] Harvard Univ, Sch Med, Radiobiol Lab, Boston, MA USA
关键词
bystander response; ionizing radiation; alpha-particles; gap-junction intercellular communication; oxidative stress;
D O I
10.1038/sj.onc.1206961
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Evidence accumulated over the past two decades has indicated that exposure of cell populations to ionizing radiation results in significant biological effects occurring in both the irradiated and nonirradiated cells in the population. This phenomenon, termed the 'bystander response', has been shown to occur both in vitro and in vivo and has been postulated to impact both the estimation of risks of exposure to low doses/low fluences of ionizing radiation and radiotherapy. Several mechanisms involving secreted soluble factors, oxidative metabolism and gap-junction intercellular communication have been proposed to regulate the radiation-induced bystander effect. Our current knowledge of the biochemical and molecular events involved in the latter two processes is reviewed in this article.
引用
收藏
页码:7050 / 7057
页数:8
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