CYTOCHROME P4501A INDEXES AS BIOMARKERS OF CONTAMINANT EXPOSURE - RESULTS OF A FIELD-STUDY WITH PLAICE (PLEURONECTES-PLATESSA) AND FLOUNDER (PLATICHTHYS-FLESUS) FROM THE SOUTHERN NORTH-SEA

Within the framework of the Integrated North Sea Programme (INP), samples of two flatfish species, flounder, Platichythys flesus, and plaice, Pleuronectes platessa, were collected during August/September 1991 and May/June 1992 in the southern North Sea. The aim of the study was to examine the induction of hepatic cytochrome P4501A (CYP1A) in both species when exposed to environmental PCBs and PAHs. Plaice and flounder occupy different but partly overlapping habitats. Flounder live mainly in estuaries and coastal areas whereas plaice can be found throughout the North Sea. CYP1A was measured by a semiquantitative immunochemical ELISA technique and also by the activity of its catalyst, 7-ethoxyresorufin O-deethylase (EROD). In plaice, both hepatic CYP1A protein level and EROD activity were significantly higher at offshore sampling locations than at coastal locations, by a factor of 1.5 to 2. In flounder, which were only collected at coastal locations, the range of values of EROD activity was much greater than in plaice, but the response in the ELISA test using polyclonal trout CYP1A1 antibodies was comparable in both species. Multiple regression analysis of data from plaice and flounder did not show any significant correlation between CYP1A indices, water temperature and contaminant concentrations in fish tissues. CYP1A indices also appeared to be unrelated to food type, as determined by visual screening of fish intestines. One possible explanation for the lack of correlation between CYP1A indices and indices of exposure to pollution could be the influence of additional modifying factors (biological, physical or chemical), which might mask CYP1A induction by PCBs and PAHs in this area. However, the low statistical power of the tests used, related to difficulties in collecting sufficiently large sample sizes, should also be borne in mind. It can be concluded that the induction of CYP1A in plaice and flounder from the southern North Sea is not related in a simple manner to exposure to PCBs and PAHs, two groups of chemicals that cause induction in the laboratory. Apparently other unknown modifying factors also have a considerable influence. From the point of view of use as a biomarker, the measurement of CYP1A protein level and EROD activity in plaice and flounder from the open North Sea cannot be applied straightforwardly for monitoring exposure to PCBs and/or PAHs in the absence of more knowledge about the mentioned modifying factors.