Response of the G2-prophase checkpoint to genotoxic drugs in lymphocytes from healthy individuals.

We analyzed the in vitro effects of the anti-tumoral drugs doxorubicin, cytosine arabinoside and hydroxyurea on the G2-prophase checkpoint in lymphocytes from healthy individuals. At biologically equivalent concentrations, the induced DNA damage activated the corresponding checkpoint. Thus: i) there was a concentration-dependent delay of G2 time and an increase of both the total DNA lesions produced and repaired before metaphase and; ii) G2-checkpoint adaptation took place as chromosome aberrations (CAs) started to appear in the metaphase, indicating the presence of unrepaired double-strand breaks (DSBs) in the previous G2.

Hepatocytes, rather than leukocytes reverse DNA damage in vivo induced by whole body gamma-irradiation of mice, as shown by the alkaline comet assay.

DNA damage repair was assessed in quiescent (G0) leukocytes and in hepatocytes of mice, after 1 and 2 hours recovery from a single whole body y-irradiation with 0.5, 1 or 2 Gy. Evaluation of single-strand breaks (SSB) and alkali-labile sites together were carried out by a single-cell electrophoresis at pH>13.

G2 checkpoint-dependent DNA repair and its response to catalase in Down syndrome and control lymphocyte cultures.

The amount of DNA lesions repaired in G2 and also G2 timing are controlled by the DNA damage-dependent checkpoint. Down syndrome (DS) lymphocytes showed twice as much constitutive DNA damage in G2 than control ones, when recording it as chromosomal aberrations in metaphase, after caffeine-induced checkpoint abrogation. During G2, DS lymphocytes repaired 1.

The G2 checkpoint activated by DNA damage does not prevent genome instability in plant cells.

Root growth, G2 length, and the frequency of aberrant mitoses and apoptotic nuclei were recorded after a single X-ray irradiation, ranging from 2.5 to 40 Gy, in Allium cepa L. root meristematic cells.

Roles of nibrin and AtM/ATR kinases on the G2 checkpoint under endogenous or radio-induced DNA damage.

Checkpoint response to DNA damage involves the activation of DNA repair and G2 lengthening subpathways. The roles of nibrin (NBS1) and the ATM/ATR kinases in the G2 DNA damage checkpoint, evoked by endogenous and radio-induced DNA damage, were analyzed in control, A-T and NBS lymphoblast cell lines. Short-term responses to G2 treatments were evaluated by recording changes in the yield of chromosomal aberrations in the ensuing mitosis, due to G2 checkpoint adaptation, and also in the duration of G2 itself.