DNA adducts, mutant frequencies, and mutation spectra in various organs of λlacZ mice exposed to ethylating agents
✍ Scribed by Edwin J. Mientjes; Anja Luiten-schuite; Esmeralda van der Wolf; Yvonne Borsboom; Angela Bergmans; Frits Berends; Paul H. M. Lohman; Robert A. Baan; Joost H. M. van Delft
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 156 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0893-6692
No coin nor oath required. For personal study only.
✦ Synopsis
To investigate tissue-specific relations between DNA versions, expected from O 2 -ethylthymine. In bone adducts and mutagenesis in vivo, llacZ transgenic marrow after ENU treatment, a maximum mutation mice were treated i.p. with N-ethyl-N-nitrosourea induction occurred at 3 days post-treatment, of (ENU), diethylnitrosamine (DEN), and ethyl meth-which 43% were GC r AT mutations and 22% were anesulphonate (EMS). In liver, bone marrow, and TA r AT mutations. This suggests that in bone marbrain DNA from mice sacrificed at several time row O 6 -EtG may be a major premutagenic lesion points after treatment O 6 -ethylguanine (O 6 -EtG) and at the 3-day time point. In liver and bone marrow, N7-ethylguanine (N7-EtG) levels were determined EMS treatment gave rise to a high level of N7-EtG as well as the mutant frequency (MF) in lacZ. In liver and a low level of O 6 -EtG but no increase in MF. DNA of ENU-and DEN-treated mice, the bulk of No adducts or mutation induction were observed in O 6 -EtG was removed at 3 days after treatment, bone marrow of DEN-treated mice. No MF increase while the MF continued to increase thereafter. This was observed in the brain of either ENU-or EMSsuggests that O 6 -EtG is not the major premutagenic treated mice, although O 6 -and N7-adducts were lesion in the liver. Indeed, sequence analysis of mu-present. Environ. Mol. Mutagen. 31:18 -31, tants showed only 24% GC r AT transitions, consis-1998