Abstract
Juvenile Atlantic cod were placed in net cages on the bottom at 20–30 m depth at four sites from the inner end of Sørfjorden (Hardanger, Western Norway), to the northern mouth of the fjord in October 1990. After 4 weeks the fish were killed, and liver samples were analyzed for aromatic and chlorinated hydrocarbons (PAHs and PCBs). Liver and gill were also analyzed for cytochrome P450 1A induction, a biomarker for exposure and effects of these contaminants, using catalytic measurements (7-ethoxyresorufin- O-deethylase, EROD) and immunodetection (P450 1A1-ELISA). The caging resulted in the accumulation of a number of PAHs, but very little PCBs, in the liver of the cod, with an inward gradient in the fjord. The gradient, although not dramatic in absolute terms, was parallelled by elevated levels of P450 1A1 when measured by EROD and, partly, by ELISA. The caging strategy seems to be a promising way to approach ecotoxicologically relevant problems, such as bioavailability of contaminants, biomarker responses in the field, and dose-response relationships, also under mixed contaminant situations.
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