Poly-D-lysine in G2 potentiates chromosome damage induced by X-rays and mitomycin C in CHO cells.

A number of reports suggest that the role of radiation-induced G2 arrest is to allow repair of potentially lethal damage in the cells before it comes to mitosis. Though the exact nature of the damage undergoing repair during the delayed G2 is not known, the yield of chromosomal aberrations observed in metaphase seems to be a good parameter to predict reproductive death of cells. In a previous paper, we have shown that poly-D-lysine, acting in a fashion reminiscent of that of caffeine in mammalian cells, is able to induce a premature onset of mitosis concomitant with an increase in the frequency of chromosomal aberrations in mutagen-treated plant cells. Cultured CHO cells were pre-exposed to either X-rays or mitomycin C and given different doses of the polycationic compound during G2 in order to analyze any effect on the frequency of chromatid-type aberrations as well as any modification of cell-cycle kinetics. A potentiation of chromosome damage and a premature arrival at mitosis were observed for both mutagens, though the effect was more evident in X-irradiated cells.