Comparison of cell inactivation by Auger electrons using the two reagents 4-[123I]iodoantipyrine and [123I]NaI |
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Authors: | Barend Schalk Smit J P Slabbert S A Reinecke L Böhm |
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Institution: | (1) National Accelerator Centre, P.O. Box 72, Faure 7131, South Africa, ZA;(2) Department of Zoology, University of Stellenbosch, Private Bag X1, Matieland 7602, South Africa, ZA;(3) Department of Radiation Oncology, University of Stellenbosch, P.O. Box 19063, Tygerberg 7505, South Africa e-mail: elb@gerga.sun.ac.za Tel.: +27-21-9389539, Fax: +27-21-9338886, ZA |
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Abstract: | The Auger electron emitter 123I was examined in the form of 4-123I]iodoantipyrine and as 123I]NaI for its effectiveness in killing cells of different sensitivity to photon irradiation. Micronucleus assays showed that
4-123I]iodoantipyrine is 2–3 times more effective in cell inactivation than 123I]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 123I]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 123I]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 4-123I]iodoantipyrine as compared to 123I]NaI is similar for all cell lines and that the ratio of 4-123I]iodoantipyrine/123I]NaI MN response remains the same. Experiments with the free radical scavenger DMSO, indicated nearly identical dose reduction
factors for both 123I carriers. These two observations strongly suggest that the cell inactivation by 4-123I]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 4-123I]iodoantipyrine is not incorporated into the DNA, but is only associated with chromatin where the DNA is shielded by histones.
Received: 24 May 2000 / Accepted: 1 November 2000 |
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