The relationship between in vivo
aneuploidy and cell-cycle perturbation induced by potential
aneugens was investigated in mouse bone marrow cells. This work was performed within the framework of a research programme coordinated by the European Community to study the ability of 10 selected chemicals to induce
aneuploidy in different systems. In this context, the effects of
colchicine (COL) and
hydroquinone (HQ) on cell-cycle progression,
aneuploidy,
polyploidy, micronucleus and sister chromatid exchange induction in mouse bone marrow cells after
bromodeoxyuridine incorporation are reported. Hyperploidy and
polyploidy were scored in metaphases of cells that had undergone only one division
after treatment. Both chemicals induced cell-cycle lengthening, hyperploidy and micronuclei. The kinetics of hyperploidy induction by the two compounds differed in that COL was positive at 24 h, whereas HQ was positive 18 h
after treatment. Only
colchicine was positive for
polyploidy induction and neither chemical induced sister chromatid exchange. These results are compared with similar data obtained after
vinblastine (VBL) treatment. The results suggest that VBL and COL induce chromosome malsegregation via a mechanism associated with perturbations in the cell-cycle, whereas HQ induces
aneuploidy independently of cell-cycle lengthening, possibly altering a chromosomal component of chromosome segregation rather than a spindle component.