Cytochrome P450IA induction by a coplanar PCB, a PAH mixture, and PCB-contaminated sediment extracts following microinjection of rainbow trout sac-fry

Abstract

The 7-ethoxyresorufin- O-deethylase (EROD)-inducing potencies of a coplanar polychlorinated biphenyl (PCB) (3,3′,4,4′,5-pentachlorobiphenyl, IUPAC No. 126), a mixture of five polycyclic aromatic hydrocarbons (benzo(k)fluoranthene, benz(a)anthracene, benzo(a)pyrene, indeno(1,2,3-cd)pyrene and chrysene), and lipophilic compounds extracted from the sediments in a PCB-contaminated lake and from sediments in lakes up- and downstream, were studied in rainbow trout sac-fry in a 43-day study. The compounds/extracts were injected into the yolk sacs of newly hatched sac-fry and hepatic EROD activities and mortality rates were measured at various times after the injections. Five livers from each group were also examined by transmission electron microscopy. All the compounds/extracts induced hepatic EROD activities in the sac-fry. Ten days after injection the EROD activity caused by PCB No. 126 (1.3 ng per embryo) was 40-fold compared to the control activity. This was the highest induction rate observed in the experiment. For the sediment extracts, the highest induction rates were observed at the first sampling occasion, which for these groups was on day 24. The extract from the Lake Järnsjön sediment was more potent as an EROD inducer than the extracts of sediments from the lakes up- and downstream from Lake Järnsjön. None of the sediment extracts caused any significant mortality. In sac-fry injected with the PAH mixture, EROD was only slightly induced. The highest dose of PAHs (10 μg per embryo) caused about 90% mortality by 24 days after injection. When the livers were examined by transmission electron microscopy, morphological alterations (e.g. hepatocyte degeneration and hypertrophy) were seen in the groups injected with Lake Järnsjön sediment extract, PCB No. 126 and the highest dose of the PAH mixture (10 μg per embryo).