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Induction of DNA Double‐Strand Breaks by <sup>157</sup>Gd Neutron Capture

Roger F. MartinMolecular Science Group, Peter MacCallum Cancer Institute, Melbourne 3000G. D'CUNHAMolecular Science Group, Peter MacCallum Cancer Institute, Melbourne 3000Marshall PardeeMolecular Science Group, Peter MacCallum Cancer Institute, Melbourne 3000Barry AllenLucas Heights Research Laboratories, Australian Nuclear Science and Technology Organisation, New South Wales, Australia
1989en
ABI

Annotatsiya

The rationale of boron ( 10 B) neutron capture therapy (BNCT) is based on the high thermal neutron capture cross section of 10 B and the limited maximum range (about one cell diameter) of the high LET fission products of the boron neutron capture (NC) reaction. The resulting radiochemical damage is confined to the cell containing the BNC reaction. Although other nuclides have higher thermal neutron capture cross sections than 10 B, NC by such nuclides results in the emission of highly penetrating gamma rays. However, gadolinium‐157 ( 157 Gd) n‐gamma reaction is also accompanied by some internal conversion and, by implication, Auger electron emission. Irradiation of Gd 3+ ‐DNA complexes with thermal neutrons results in the induction of DNA double‐strand (ds) breaks, but the effect is largely abrogated in the presence of EDTA. Thus, by analogy with the effects of decay of Auger electron‐emitting isotopes such as 125 I, the Gd NC event must take place in the close proximity of DNA in order to induce a DNA ds break. It is proposed that 157 Gd‐DNA ligands therefore have potential in NCT. The thermal neutron capture cross section of 157 Gd, a nonradioactive isotope, is more than 50 times that of 10 B.

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