Abstract
Administration of β-naphthoflavone (BNF) intraperitoneally to scup ( Stenotomus chrysops) increased the specific content of total cytochrome P-450 (P-450) in gill microsomes nearly ten-fold. This increase in P-450 content was accompanied by an increase in microsomal ethoxyresorufin O-deethylase activity from undetectable levels to 0.16 nmol/min/mg, and a shift in the Fe 2+-CO absorption maximum from 450 to 447 nm. Western blot analysis of microsomes from control and BNF-treated scup gills, with monoclonal antibody (MAb) 1-12-3 directed against scup P-450E (the BNF-inducible EROD catalyst), confirmed that P-450E was induced from undetectable levels in control animals to levels comprising at least 60% of the spectrally measured gill P-450 in BNF-treated animals. Immunohistochemical analysis of scup gills with MAb 1-12-3 as primary antibody showed that the P-450E was induced primarily in the endothelium (pillar cells) of the secondary lamellae. Immunohistochemical analysis of gills from rainbow trout ( Salmo gairdneri) showed that BNF treatment also induced a P-450E counterpart in trout gills and that, as in scup, this P-450 was localized principally in the endothelium of gill lamellae. P-450E catalyzes formation of promutagenic benzo-ring dihydrodiols of benzo[ a]pyrene, which suggests possible toxicological consequences for the induction of this isozyme in gill.
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