Bioavailability to juvenile rainbow trout (Oncorynchus mykiss) of retene and other mixed-function oxygenase-active compounds from sediments.

Retene (7-isopropyl-1-methylphenanthrene) is a naturally formed polycyclic aromatic hydrocarbon (PAH) that causes teratogenicity in fish larvae and induction of cytochrome P450 (CYP1A) enzymes. Retene occurs at high concentrations (< or =3,300 microg/g dry wt) in surface sediments contaminated by resin acids from pulp mill effluents. To assess the environmental risks of retene, it is important to evaluate conditions affecting its bioavailability and accumulation by fish. Fingerling rainbow trout were exposed to retene-spiked or naturally contaminated sediments and sampled after 4 d to determine liver CYP1A activity and concentrations of retene metabolites in bile as indicators of retene accumulation. Industrially contaminated sediments collected near a bleached kraft pulp and paper mill discharging to Lake Saimaa, Finland, significantly induced trout liver CYP1A activity, indicating accumulation of arylhydrocarbon receptor (AhR)-active ligands. Bile of these fish contained retene metabolites, providing direct evidence that retene is bioavailable, presumably via desorption from sediments. Induction of CYP1A in fish exposed to sediments spiked with retene or benzo[k]fluoranthene supported this conclusion. While the extent of CYP1A induction by spiked sediments declined after storage (i.e., aging), a portion of the spiked PAHs remained bioavailable. However, retene was not the sole CYP1A inducer in industrially contaminated sediments, as shown by induction in fish injected with sediment extracts oxidized to remove labile PAHs but not persistent organochlorine compounds such as chlorinated dioxins and furans.