The Japan Radiation Research Society Annual Meeting Abstracts
The 52nd Annual Meeting of the Japan Radiation Research Society
Session ID : OC-14
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Carcinogenesis 2
Intervention of mitochondrial function to the cell transformation route, which assumes aneuploid driving force
*Masami WATANABEHanako YOSHIIKimiko WATANABEHisakatsu NAWATAKeizo TANOGenro KASHINOJun KUMAGAI
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CONFERENCE PROCEEDINGS FREE ACCESS

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Abstract

We have proposed a new route of in vitro cell transformation, which assumes aneuploid driving force. This route does not originated from DNA lesion origin, but it is thought that it is the main route of cell transformation. A main target of this route may be centrosome, and disorder of centrosome causes chromosomal non-disjunction and aneuploid. From the results of research with mouse embryo cell and Syrian hamster embryo cells, intracellular oxidation radical which an electron to leak from mitochondria generates may become a trigger of both natural- and radiation-induced cell transformation. Intracellular oxidation radical and the derivation radical of a high level induce dysfunction of centrosome, and centrosome dysfunction causes aneuploidy. These results suggest that the route of radiation-induced cell transformation may be the same as that produced by natural physiology action. Alternatively, this means that physiological threshold is present in low dosage area in cell transformation.

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© 2009 The Japan Radiation Research Society
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