Juvenile sea bass liver biotransformation and erythrocytic genotoxic responses to pulp mill contaminants.

This research represents the first study concerning liver phase I biotransformation induction, measured as cytochrome P-450 (P450) and ethoxyresorufin-O-deethylase (EROD), and genotoxic responses, measured as erythrocytic micronuclei (EMN) and nuclear abnormalities (ENA), in Dicentrarchus labrax L. (sea bass) exposed to pulp and paper mill contaminants. Juvenile sea bass were exposed for 6 h to 0 (control) and 0.0125 microM concentrations of the resin acids (RAs) abietic acid (AA) and dehydroabietic acid (DHAA) or 7-isopropyl-1-methylphenanthrene (retene) (Experiment 1). Sea bass were exposed for 6 h to 0 (control), 0.78, 1.56, 3.12, 6.25, and 12.5% bleached kraft pulp mill environmental contaminated water (BKPMECW) collected at the old sewage outlet of a pulp and paper industry (Experiment 2). The time-dependent response was studied in sea bass at 0, 8, 16, 24, 48, and 72 h exposure to 0.78 and 12.5% BKPMECW (Experiment 3). The experimental results demonstrated the presence of genotoxic compounds in BKPMECW. AA, DHAA, and retene may be the constituents responsible for high BKPMECW genotoxicity, since they induced similar sea bass EMN and ENA frequency increases. The BKPMECW, the RAs, and retene failed to significantly increase liver EROD activity and P450 content at 6 h. Furthermore, 3.12% BKPMECW, 0.0125 microM AA, and 0.0125 microM retene significantly decreased liver EROD activity. However, P450 was significantly increased from 8 up to 72 h exposure to BKPMECW. Therefore, the low or inhibited EROD levels could be a consequence of a general membrane disturbance by BKPMECW, RAs, and retene. However, liver ALT results indicate significant liver damage or enzyme inhibition only at 8, 16, 48, and 72 h exposure to BKPMECW.