الفهرس | Only 14 pages are availabe for public view |
Abstract Repair—defective mutants of Drosophila nielanogaster have been used to find a probable relationship between the genetic damage induced by alkylating agents and DNA—repair. The sex—linked recessive lethals and sex—chromosome loss were used as measures of genotoxic endpoints. The alkylating agents tested were MMS, EMS, DMN and DEN. The sex—linked recessive lethal test was used to compare mutation induction by EMS or DEN in mature sperm and late spermatid stages of the DNA repair deficient mci_gd (excision—repair—deficient) mutant and the repair proficient control strain. For both agents, the data demonstrate that induced mutation rates were almost the same in both strains. The data were interpreted as that excision repair processes for alkylation damage are inactive in post—iueiotic germ cell stages. When repair proficient males (M—5) were treated with the four alkylating agents and mated with mel_ga females or with appropriate Berlin wild females, the frequencies of recessive lethals induced with mci_ga females were higher than those induced with Berlin wild females. The data are explained as follows: excision repair deficiencies cause the processing of primary lesions to be derived from the error— prone pathways. Repair proficient males (M—5) were treated with PINS and DMN and mated with mei_41D5 females (post—replication— repair—deficient) or flerlin wild females. The frequencies of |