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Mutagenesis vol. 19 no. 2 pp. 121-127, March 2004
© 2004 UK Environmental Mutagen Society/Oxford University Press

Detection of mitotic recombination and sex chromosome loss induced by adriamycin, chlorambucil, demecolcine, paclitaxel and vinblastine in somatic cells of Drosophila melanogaster in vivo

Rosario Rodríguez-Arnaiz1, América Castañeda Sortibrán and Guadalupe Ordaz Téllez

Laboratorio de Genética, Facultad de Ciencias, UNAM, Coyoacán, 04510 México, DF México

The conventional w/w+ eye assay in Drosophila has been used for the last 10 years for genotoxic evaluation of a broad number of chemicals with different mechanisms of action. Although chemicals that induce genotoxic effects by mechanisms other than covalent binding to DNA are difficult to detect. The aim of this study was the parallel detection of both mitotic recombination and X chromosome loss induced by five chemical compounds used worldwide as antineoplastic drugs using the w/w+ somatic assay in Drosophila melanogaster. The compounds tested were the intercalating agent adriamycin (AD), the alkylating compound chlorambucil (CAB) and the spindle poisons demecolcine (DEM), paclitaxel (taxol, TX) and vinblastine (VBL). We used a cross between heterozygous females with a rod-X and a ring-X chromosome mated with ywf males. All four genotypes in the next generation are heterozygous or hemizygous for the w+ reporter gene and were inspected for the occurrence of white clones in their compound eyes. We found differences in the induction of mitotic recombination when compared with chromosome loss. Genotoxic profiles obtained for the antineoplastic drugs studied indicate direct and indirect effects. While AD seems to be clastogenic due to its induction of X chromosome loss in XrX females; DEM, CAB and TX produced both structural chromosome aberrations through clastogenic activities and mitotic recombination through DNA interactions; the cytotoxic VBL induced rX loss only in XrY and intra-chromosomal recombination (XY) males, probably due to sister strand recombination, generating a w+w+ duplication and a w deletion, forward mutations or small deletions at the white locus.

1To whom correspondence should be addressed. Tel: +52 5 622 4906; Fax: +52 5 622 4828; Email: rra{at}hp.fciencias.unam.mx

Received on 21 July 2003; revised on 12 November 2003; accepted on 14 November 2003


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