GENETIC TOXICITY IN DAB LIMANDA-LIMANDA FROM THE NORTH-SEA

During the Bremerhaven Workshop, a battery of assays was employed aimed at the detection of genetic damage in dab Limanda limanda and at an understanding of the influence of pollution on the metabolism of chemical pro-mutagens. The presence of chemical/DNA adducts was investigated by P-32-postlabelling (for bulky hydrophobic adducts) and by HPLC with electrochemical detection (for oxidised deoxyguanosine). No significant differences were seen between the various sites analysed along the transect. Bacterial mutagenicity assays (Salmonella typhimurium strains TA100 and TA98) were also unable to detect frame-shift or base-pair mutagens in liver extracts or in bile samples following treatment with the deconjugating enzyme, beta-glucuronidase. There was no evidence of pollution-related unscheduled DNA synthesis in dab hepatocytes on the day after sampling. Unscheduled DNA synthesis was, however, induced by nitroquinoline oxide (but not 2-acetylaminofluorene) in dab hepatocytes from 2 stations of different pollution status. The extent of excision repair was similar at the 2 stations. Regarding the metabolism of pro-mutagens, liver enzymes were capable of converting 2-acetylaminofluorene to bacterial mutagens; a process requiring N-hydroxylation and deacetylation. The activation ability was greater in fish from the polluted stations (3 & 5) relative to Stns 6 & 7, and this may reflect the findings of others on cytochrome P450 induction.