Caprolactam induces genetic alterations in early germ cell stages and in somatic tissue of D. melanogaster.
The ability of caprolactam (CAP) to induce somatic mutation/mitotic recombination (SMART) in heterozygous white/white-coral female larvae was examined in comparison with 2 assays measuring sex-linked recessive lethals (SLRL) in male and female larvae. The overall result is a positive response in both the SMART and SLRL assays after treatment of female genotypes, indicating that CAP acts as a weak genotoxin in Drosophila. The SLRL assay on male larvae was devoid of any activity. This finding is consistent with the view that an intrinsic limitation to assays measuring heritable genetic damage in premeiotic cell stages, particularly in hemizygous condition as in males, is that mutational events in those cells may be eliminated either by repair, by selection, or by both mechanisms. Thus the failure of CAP to elicit mutagenic activity in premeiotic male cells could be interpreted to mean that in Drosophila as in human lymphocytes, CAP acts as a clastogenic cell mutagen.
Vogel
E W
EW
Department of Radiation Genetics and Chemical Mutagenesis, Sylvius Laboratories, State University of Leiden, The Netherlands.
D000818:Animals; D001381:Azepines / Q000633:toxicity*; D002209:Caprolactam / Q000633:toxicity*; D004331:Drosophila melanogaster / Q000235:genetics*; D005260:Female; D005804:Genes, Lethal; D005808:Genes, Recessive; D005854:Germ Cells / Q000187:drug effects*; D007814:Larva / Q000187:drug effects; D008297:Male; D009153:Mutagens
D001381:Azepines; D009153:Mutagens; D002209:Caprolactam