Communication of Radiation-Induced Signals in Vivo between DNA Repair Deficient and Proficient Medaka (Oryzias latipes)

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• 作者：C. Mothersill ; R. W. Smith ; T. G. Hinton ; K. Aizawa ; C. B. Seymour
• 刊名：Environmental Science & Technology
• 出版年：2009
• 出版时间：May 1, 2009
• 年：2009
• 卷：43
• 期：9
• 页码：3335-3342
• 全文大小：226K
• 年卷期：v.43,no.9(May 1, 2009)
• ISSN：1520-5851

文摘

Radiation-induced bystander effects are established consequences of exposure to ionizing radiation. The operation of this mechanism has been seen in vitro and also between fish, mammals, and plants in vivo where stress signals from treated organisms induce responses in neighbors. In vitro research shows that DNA repair deficient cells produce more toxic bystander responses. To test this in vivo two strains of Japanese medaka were tested. One is a mutant, repair deficient strain (ric2) and the other, the wildtype repair proficient strain (CAB). Irradiated fish swam with unirradiated partners in a strain mix and match protocol. The data suggest that medaka produce signals, when exposed to radiation, that induce unirradiated fish of the same strain swimming with them to produce an altered response to that seen in bystanders to sham irradiated fish. More apoptosis was seen in bystanders to repair deficient fish. When the strains are mixed, the bystanders of either strain respond like the donor strain. Measurements of Bcl-2 and cmyc proteins in the explants confirmed these observations. A possible role for p53 was also identified in that the use of reporters with mutant p53 demonstrated that CAB signals killed all the reporter cells by apoptosis. Use of a similar but p53 wild-type cell line had no such effect. The data add to the body of knowledge showing that bystander signals operate at hierarchical levels of organization greater than the individual and may therefore have relevance in radioecology and (eco)systems biology.