PUBLICATION
Mutational spectra of benzo[a]pyrene and MeIQx in rpsL transgenic zebrafish embryos
- Authors
- Amanuma, K., Tone, S., Saito, H., Shigeoka, T., and Aoki, Y.
- ID
- ZDB-PUB-011126-1
- Date
- 2002
- Source
- Mutat. Res. Genet. Toxicol. Environ. Mutagen. 513(1-2): 83-92 (Journal)
- Registered Authors
- Amanuma, Kimiko, Aoki, Yasunobu
- Keywords
- transgenic zebrafish; rpsL; benzo[a]pyrene; MeIQx
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Benzo(a)pyrene/toxicity*
- Mutagens/toxicity*
- Mutation*
- Quinoxalines/toxicity*
- Ribosomal Proteins/genetics*
- Zebrafish/genetics*
- PubMed
- 11719093 Full text @ Mutat. Res. Genet. Toxicol. Environ. Mutagen.
Citation
Amanuma, K., Tone, S., Saito, H., Shigeoka, T., and Aoki, Y. (2002) Mutational spectra of benzo[a]pyrene and MeIQx in rpsL transgenic zebrafish embryos. Mutat. Res. Genet. Toxicol. Environ. Mutagen.. 513(1-2):83-92.
Abstract
To evaluate the rpsL transgenic zebrafish (Brachydanio rerio) mutation assay, we treated the embryos with benzo[a]pyrene (B[a]P) (10μg/ml) or 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) (300μg/ml) for 16h and determined the mutation spectra. These treatments were previously reported to induce mutant frequencies that were 4.3 and 2.4 times the control value, respectively. In the B[a]P-treated group, half of the mutations were single base substitutions, 74% of which occurred at G:C base pairs. Among G:C base pair substitutions, G:C to T:A and G: C to C:G transversions were predominant, suggesting that B[a]P induced mutations in zebrafish embryos by mechanisms previously described in mammalian tissues. In the MeIQx-treated group, about 60% of the mutations were deletions. Some specific mutations were found, but the compound primarily amplified the background mutation level; improvement in the conditions of treatment may be required for elucidating MeIQx-mutagenesis in this system. This study showed that transgenic zebrafish may be a useful tool for detecting mutagens in aquatic environments and for elucidating mutagenic mechanisms.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping