Abstract
The prediction ability of a test to detect genotoxic activity may be increased, at least from a theoretical point of view, by carrying it out under deficient repair conditions. The white-ivory (w[i]) assay of Drosophila melanogaster is a somatic mutation and recombination test (SMART) that essentially differs from other SMARTs by the endpoints that can be detected. In this article, we study the consequences, with the w(i) assay, of the introduction of two mutations, mus201 and mei-41, which produce deficiency in two different repair mechanisms: the nucleotide excision repair system and in a G2/M cell-cycle checkpoint, respectively. Ten chemicals, previously classified as positive in the w(i) assay, have been assayed in both deficient repair conditions. As in the w/w+ and mwh/flr3 SMARTs, the results obtained with the w(i) assay show that the use of deficient repair strains does not improve the detection of genotoxic effects. However, the utilization of these deficient repair strains has been shown to be a useful tool in mechanistic studies. In fact, it seems that the nucleotide excision repair system mainly eliminates some spontaneous and chemically-induced damages involved in the reversion of w(i), whereas the repair system deficient in mei-41 flies is partly necessary to recover revertant w(i) spots.
