Benzo[a]pyrene and beta-naphthoflavone mutagenic activation by European eel (Anguilla anguilla L.) S9 liver fraction
Is Anguilla anguilla L. (eel) liver ethoxyresorufin O-deethylase (EROD) induction absolutely necessary in order to convert promutagens as benzo[a]pyrene (BaP) into a mutagenic compound? Eels were exposed for 8 h to clean (control) and 0.3 microM beta-naphthoflavone (BNF)-contaminated water. The 8-h...
| Published in: | Ecotoxicology and Environmental Safety |
|---|---|
| Main Authors: | , , |
| Format: | Article in Journal/Newspaper |
| Language: | English |
| Published: |
Elsevier
2002
|
| Subjects: | |
| Online Access: | http://hdl.handle.net/10773/27582 https://doi.org/10.1006/eesa.2001.2204 |
| Summary: | Is Anguilla anguilla L. (eel) liver ethoxyresorufin O-deethylase (EROD) induction absolutely necessary in order to convert promutagens as benzo[a]pyrene (BaP) into a mutagenic compound? Eels were exposed for 8 h to clean (control) and 0.3 microM beta-naphthoflavone (BNF)-contaminated water. The 8-h exposure to 0.3 microM BNF brought about a very high EROD induction (10 pmol/min/mg protein) compared to control animals (1 pmol/min/mg protein). The Ames test (Maron and Ames, 1983) was carried out with Salmonella typhimurium TA 98 strain (TA98 His-) and eel isolated S9 liver fraction was used as a metabolic BaP activator. The BaP and BNF dose range concentrations tested were 0 (blank), 0.015, 0.08, 0.15, 0.38, 0.75, 1.5, 3.8, and 7.5 microM/plate and 0 (blank), 0.412, 1.235, 3.704, 11.1, 33.0, and 100 nM BNF, respectively. A dose-response relationship between BaP concentration and mutagenic activity was observed in the presence of S9 fractions in control and 0.3 microM BNF-exposed eels. Significant positive results, as TA98 His+ revertants, were observed at 0.38, 0.75, 1.5, 3.8, and 7.5 microM BaP/plate induced by BNF S9 fractions. Significant BaP mutagenic activation by liver control S9 was detected only at 1.5, 3.8, and 7.5 microM/plate. The BaP 1.5, 3.8, and 7.5 microM/plate mutagenic activation by BNF S9 and control S9 were not significantly different. Relative to BNF activation, it was only possible to detect His+ reversion at 11.1 nM BNF concentration with 0.3 microM BNF-induced S9. The above results demonstrate that the eel S9 liver fraction has the capacity to biotransform high BaP concentrations and convert it into a mutagenic compound with or without previous liver BNF biotransformation induction. The same does not apply to low BaP concentrations, where liver S9 induction by BNF is necessary to promote mutagenesis. published |
|---|