Origin of aneuploidy in relation to disturbances of cell-cycle progression. II: Cytogenetic analysis of various parameters in mouse bone marrow cells after colchicine or hydroquinone treatment.

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.