期刊
RADIATION PROTECTION DOSIMETRY
卷 99, 期 1-4, 页码 227-232出版社
NUCLEAR TECHNOLOGY PUBL
DOI: 10.1093/oxfordjournals.rpd.a006769
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- NCI NIH HHS [CA 75384, CA 49062] Funding Source: Medline
- NCRR NIH HHS [RR 11623] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA049062, R01CA075384] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P41RR011623] Funding Source: NIH RePORTER
It has always been accepted dogma that the deleterious effects of ionising radiation such as mutagenesis and carcinogenesis are due mainly to direct damage to DNA. Using the Columbia University charged-particle microbeam, and the highly sensitive A(L) Cell mutagenic assay, it is shown here that non-irradiated cells acquire the mutagenic phenotype through direct contact with cells whose nuclei are traversed with 2 alpha particles each. Pre-treatment of cells with lindane, a gap junction inhibitor, significantly decreased the mutant yield, Furthermore, when irradiated cells were mixed with control cells in a similar ratio as the in situ studies, no enhancement in bystander mutagenesis was detected, Our Studies provide clear evidence that genotoxic damage can be induced in non-irradiated cells, and that gap junction mediated cell-cell communication plays a critical role in the bystander phenomenon.
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