Juvenile Sea Bass Liver P450, EROD Induction, and Erythrocytic Genotoxic Responses to PAH and PAH-like Compounds

Abstract

Sea bass were exposed, for 0, 2, 4, 6 and 8 h, to 0 or 2.7 μM β-naphthoflavone (BNF), or to 0, 0.1, 0.3, 0.9, or 2.7 μM benzo[a]pyrene (B(a)P) and naphthalene (NAPH). Liver cytochrome P-450 content (P450) and liver ethoxyresorufin-O-deethylase activity (EROD) induction were determined as phase I biotransformation responses, whereas erythrocytic micronuclei (EMN) and erythrocytic nuclear abnormalities (ENA) tests were performed to assess genotoxic effects. Liver alanine aminotransferase activity and liver somatic index were determined, respectively, as liver damage and common health indicators. A significant increase in sea bass EROD activity began, respectively, at 2 and 4 h exposure to 2.7 μM B(a)P and 2.7 μM BNF, whereas NAPH failed to induce EROD activity. Maximal EROD activity was observed after 6 h exposure to 2.7 μM BNF (9-fold increase), 2.7 μM B(a)P (4-fold increase), and 2.7 μM NAPH (2-fold increase), indicating BNF as the most potent EROD inducer (BNF>B(a)P>NAPH). A significant increase in liver P450 content was observed at 6 h exposure to 2.7 μM BNF (6.5-fold increase), indicating BNF as the most potent P450 inducer. A significant P450 increase was observed at 8 h exposure only to 0.1 μM B(a)P (2-fold increase), whereas it slightly increased at 2 h exposure to 2.7 μM NAPH, within a wide variable range. The BNF, NAPH, and B(a)P genotoxic potential was demonstrated as sea bass EMN and ENA. B(a)P promoted at 2 h exposure a significant EMN (24-fold) and ENA (2.2-fold) increase, whereas NAPH exhibited similar results only at 8 h exposure. BNF also increased significantly sea bass EMN (8-fold) and ENA (1.5-fold) after 8 h. The results indicated B(a)P as the most genotoxic compound, followed by NAPH and BNF (B(a)P>NAPH>BNF). Despite the low liver P450 content and EROD activity induction by NAPH and B(a)P, their genotoxic potential was higher than that of BNF.