Abstract

Hydroxyurea (HU) is an inhibitor of DNA synthesis, which can inhibit the enzyme ribonucleotide reductase, reduce the syntheses of all four deoxyribonucleoside diphosphates (dNDP), and disturb the balance of the dNTP pool. We have studied the effect of HU on the common fragile site at 3p14 (FRA3B) and have found that G2 treatment with HU increased not only the frequency of chromosomal aberration but also the expression of FRA3B in both complete and folate deficient media. There is a synergistic effect between HU and growth in folate deficient medium on the induction of FRA3B. Our results suggest that the inhibition of DNA repair, including the inhibition in G2 phase, plays an important role in the expression of FRA3B, supporting other authors' data on the effect of other DNA repair inhibitors, such as aphidicolin, caffeine, 1-beta-D-arabinofuranosylcytosine, and 5-fluorodeoxyuridine, on the expression of FRA3B.