DNA adduct formation and persistence in liver and extrahepatic tissues of northern pike (Esox lucius) following oral exposure to benzo[a]pyrene, benzo[k]fluoranthene and 7H-dibenzo[c,g]carbazole.
The formation and persistence of DNA adducts in liver, intestinal mucosa, gills and brain of juvenile northern pike (Esox lucius) following oral exposure to benzo[a]pyrene (BaP), benzo[k]fluoranthene (BkF) and 7H-dibenzo[c,g]carbazol (DBC) were analysed by 32P-postlabelling. The dosage was 25 micromol/kg body weight of each substance, administered on 5 occasions with an interval of 12-14 days. Sampling was carried out 9 days after the second treatment, and 9, 16, 33 and 78 days after the fifth treatment. Pikes were also fed with the substances singly for comparison of adduct patterns. A complex pattern of adducts was detected in all examined tissues from fish treated with the mixture. Total adduct levels were highest in intestine (347+/-17.4 nmol adducts/mol nucleotides, mean+/-SE), followed by liver (110+/-9.3), gills (69+/-6) and brain (14+/-4.2). In pike treated with BaP alone, one major adduct was detected in all examined tissues. This BaP-adduct made up approximately 50% of the total amount of adducts in the brain. Corresponding values in liver, intestine and gills were 23, 31 and 34%, respectively. One relatively weak BkF-adduct and at least 10 different DBC-adducts were detected in all analysed tissues. Total adduct level in the intestine declined to 29.4% of the maximum value 78 days after the last exposure, while there was no significant decline in adduct levels in liver, gills or brain. The results suggest that intestine is more susceptible to adduct formation than liver after oral exposure, and that adduct levels in the intestine represent ongoing or relatively recent exposure. DNA adducts in the other investigated tissues were much more persistent and may therefore accumulate during long-term exposure.
Institute of Applied Environmental Research, Laboratory for Aquatic Ecotoxicology, Stockholm University, S-10691, Stockholm, Sweden. gunilla.ericson@itm.su.se
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G
Ericson
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Noaksson
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Balk
D000284:Administration, Oral; D000818:Animals; D001564:Benzo(a)pyrene / Q000009:adverse effects*; D001921:Brain / Q000378:metabolism; D002227:Carbazoles / Q000009:adverse effects*; D002273:Carcinogens / Q000009:adverse effects*; D002855:Chromatography, Thin Layer; D019363:Cytochrome P-450 CYP1A1 / Q000096:biosynthesis; D018736:DNA Adducts / Q000032:analysis*; D017859:Esocidae / Q000378:metabolism*; D005449:Fluorenes / Q000009:adverse effects*; D005880:Gills / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D013997:Time Factors; D014877:Water Pollution, Chemical / Q000009:adverse effects*
D002227:Carbazoles; D002273:Carcinogens; D018736:DNA Adducts; D005449:Fluorenes; D001564:Benzo(a)pyrene; D019363:Cytochrome P-450 CYP1A1; C013478:7H-dibenzo(c,g)carbazole; C022921:benzo(k)fluoranthene