The influence of DNA inhibitor synthesis on the induction and repair of double-strand DNA breaks in human lymphocytes under action of radiation with a different linear energy transfer |
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Authors: | A V Boreyko V N Chausov E A Krasavin I Ravnachka S I Stukova |
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Institution: | 1.Joint Institute for Nuclear Research,Dubna, Moscow oblast,Russia |
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Abstract: | The influence that inhibitors of repair and replicative DNA synthesis, 1-β-D-arabinofuranosyl-cytosine and hydroxyurea, have
on the formation and repair kinetics of double-strand breaks (DSBs) in peripheral human blood lymphocytes under the influence
of radiation with a different linear energy transfer (LET) (gamma quanta and accelerated heavy ions) is studied. It is demonstrated
that lithium and boron ions with LETs of 20 and 40 keV/μm, respectively, possess higher biological effectiveness with respect
to the DNA DSB induction criterion. The value of the relative biological effectiveness of accelerated lithium and boron ions
is 1.5 ± 0.1 and 1.6 ± 0.1, respectively. It is found that, upon cell irradiation by gamma quanta in the absence of inhibitors,
efficient DNA DSB repair is observed during incubation. Under the conditions of cell incubation and in the presence of inhibitors,
some growth in the number of DNA DSBs, rather than a reduction, is observed after 5-h incubation. In the case of the action
of accelerated boron ions (as well as gamma quanta), under normal conditions, the efficient repair of induced DNA lesions
takes place. Unlike the action of gamma quanta, in the case of cell incubation in the presence of radiomodifiers, the number
of induced DNA DSBs falls. These results may testify to the fact that the repair of double-strand DNS breaks takes place under
the action of ionizing radiation with a different LET on mammalian cells in the presence of DNA synthesis inhibitors Ara-C
and HU. It is concluded that, for cells subject to gamma irradiation, no DNA DSB repair is observed due to the large contribution
of single-strand incision DNA breaks formed in the postradiation period in the course of excision nucleotide repair. |
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