G2 repair and chromosomal damage in lymphocytes from workers occupationally exposed to low-level ionizing radiation

The effect of the G2 repair of chromosomal damage in lymphocytes from workers exposed to low levels of X- or g-rays was evaluated. Samples of peripheral blood were collected from 15 radiation workers, 20 subjects working in radiodiagnostics, and 30 healthy control donors. Chromosomal aberrations (CA) were evaluated by scoring the presence of chromatid and isochromatid breaks, dicentric and ring chromosomes in lymphocytes with/without 5mM caffeine plus 3mM-aminobenzamide (3-AB) treatment during G2. Our results showed that the mean value of basal aberrations in lymphocytes from exposed workers was higher than in control cells (p< 0.001). The chromosomal damage in G2, detected with caffeine plus 3-AB treatment was higher than the basal damage (untreated conditions), both in control and exposed populations (p< 0.05). In the exposed workers group, the mean value of chromosomal abnormalities in G2 was higher than in the control (p< 0.0001). No correlation was found between the frequency of chromosome type of aberrations (basal or in G2), and the absorbed dose. Nevertheless, significant correlation coefficients (p< 0.05) between absorbed dose and basal aberrations yield (r = 0.430) or in G2 (r = 0.448) were detected when chromatid breaks were included in the total aberrations yield. Under this latter condition no significant effect of age, years of employment or smoking habit on the chromosomal aberrations yield was detected. However, analysis of the relationship between basal aberrations yield and the efficiency of G2 repair mechanisms, defined as the percentage of chromosomal lesions repaired in G2, showed a significant correlation coefficient (r = -0.802; p< 0.001). These results suggest that in addition to the absorbed dose, the individual G2 repair efficiency may be another important factor affecting the chromosomal aberrations yield detected in workers exposed to low-level ionizing radiation

G2 repair and evaluation of the cytogenetic damage induced by low doses of X-irradiation during G0 in human lymphocytes [published erratum appears in Biol Res 1996; 29(1): 165]

In the present study two cytogenetic parameters were used to evaluate the DNA damage induced by low doses (1 up to 40 rad) of X-ray irradiation in G0 human lymphocytes. These parameters were the frequency of chromosomal lesions in G2 and the length of this cell cycle phase. The frequency of chromosomal lesions in G2 was determined by scoring the number of chromosomal aberrations in G0 irradiated lymphocytes post treated with two inhibitors of G2 repair mechanisms: caffeine and 3-aminobenzamide. A dose-dependent increase in chromosomal aberrations yield was detected in G0 lymphocytes X-ray irradiated with or without post treatment with these two DNA repair inhibitors during G2. Nevertheless, the dose response in this latter condition was higher than the one detected in control cells, indicating that the increase of irradiation dose in G0 lymphocytes produces an increment in the number of DNA lesions arriving to be repaired in G2. The analysis of the dose-response relationships for G2 length showed an statistically significant X-ray dose-dependent increase (G2 delay) from 2.5 up to 40 rad and a positive correlation between G2 delay and the frequency of chromosomal lesions in G2. These results suggest that the DNA lesions induced by low doses of X-irradiation in G0 lymphocytes may be higher than that detected by the standard method (control conditions) and may be responsible for an increase in G2 length. We propose, therefore, that an analysis of these two cytogenetic parameters can improve the evaluation of the DNA damage induced by low doses of X-rays irradiation in G0 cells

Synergistic effect of heat-shock and UV-irradiation on mitosis and protein synthesis in G2-phase plasmodia of Physarum polycephalum Schw--reduction in UV-induced mitotic delay in a preheat-shocked system.

The synergistic effect of UV irradiation and heat-shock during the last 3 hr of G2 phase of the cell cycle in the plasmodia of P. polycephalum, in terms of mitotic delay and inhibition of protein synthesis, has been evaluated. The mitotic delay due to both perturbers coordinately increased closer to mitosis. Maximum mitotic delay was obtained in plasmodia heat-shocked after UV irradiation, indicating the presence in this system of either a heat-labile mitogenic substance which is comparatively less susceptible to UV or a substance which is made more susceptible to hyperthermia by UV. A protective role for heat-shock applied before irradiation has been observed in that, radiation-induced mitotic delay is significantly reduced in this combination. There was severe inhibition of translation in all the perturbed classes. Organelle level effects which are independent of major protein synthetic activities or different levels of heat-shock protein production could be the reason for the lack of correlation between percentage inhibition of general protein synthesis and the extent of mitotic delay with respect to the two double-perturbed systems.