A deficiency for nucleotide excision repair strongly potentiates the mutagenic effectiveness of methyl bromide in Drosophila.

A DNA repair assay measuring hypermutability response in the absence of nucleotide excision repair (NER) was employed to study the impact of a deficiency in NER on the induction of forward mutations (X-chromosomal recessive lethals) by methyl bromide (MeBr) in Drosophila melanogaster. Postmeiotic male germ-cell stages reacted with MeBr were introduced in either NER competent oocytes (exr+) or in cells from the NER- strain mus-201. The high average M(exr-)/M(exr+) hypermutability ratio of 8.3 determined for MeBr is similar to the M(exr-)/M(exr+) indices found for other monofunctional alkylating agents with high Swain-Scott s values, such as methyl methanesulphonate and dimethyl sulphate. It is concluded that the genotoxic profile of methyl bromide is in keeping with those of high s-value alkylating agents but it seems incompatible with a methylating agent producing substantial amounts of O6 methylguanine.