Journal
RADIATION AND ENVIRONMENTAL BIOPHYSICS
Volume 40, Issue 1, Pages 47-52Publisher
SPRINGER-VERLAG
DOI: 10.1007/s004110000083
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The Auger electron emitter I-123 was examined in the form of 4-[I-123]iodoantipyrine and as [I-123]NaI for its effectiveness in killing cells of different sensitivity to photon irradiation, Micronucleus assays showed that 4 [I-123]iodoantipyrine is 2-3 times more effective in cell inactivation than [I-123]NaI. This can be attributed to the fact that antipyrine, for reason of its lipid solubility, can enter cells and can reach the nucleus, whereas [I-123]NaI is excluded from the cytoplasm. In the nucleus Auger decay is conceivably located on the DNA where it may invoke high-LET irradiation damage. Irradiation damage by [I-123]NaI is by long range Auger and internal conversion electrons and hence less densely ionising, Results of the present study demonstrate, however, that the enhancement of micronuclei frequency (MNF) seen with 4-[I-123]iodoantipyrine as compared to [I-123]NaI is similar for all cell lines and that the ratio of 4-[I-123]iodoantipyrine/[I-123]NaI MN response remains the same. Experiments with the free radical scavenger DMSO, indicated nearly identical dose reduction factors for both I-123 carriers. These two observations strongly suggest that the cell inactivation by 4-[I-123]iodoantipyrine is not by direct high-LET ionisation of DNA, but is due to an indirect effect. The indirect radiation effect of Auger decay in the nucleus could arise because 4-[I-123]iodoantipyrine is not incorporated into the DNA, but is only associated with chromatin where the DNA is shielded by histones.
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