Hughes EM ; Gallagher EP ;

Marine Environmental Research vol. 58 (2-5)   pp. 675-9, 2004

Department of Physiological Sciences and Center for Environmental and Human Toxicology, University of Florida, P.O. Box 110885, Gainesville, FL 32611-0885, USA.

We are investigating the effects of in vivo exposure of prototypical enzyme inducing agents on hepatic biotransformation enzyme expression in largemouth bass (Micropterus salmoides), a predatory game fish found throughout the United States and Canada. The current study targeted those genes involved in biotransformation and oxidative stress that may be regulated by Ah-receptor-dependent pathways. Exposure of bass to beta-naphthoflavone (beta-NF, 66 mg/kg, i.p.) elicited a 7-9-fold increase in hepatic microsomal cytochrome P4501A-dependent ethoxyresorufin O-deethylase (EROD) activities, but did not affect cytosolic GST catalytic activities toward 1-chloro-2,4-dinitrobenzene (CDNB) or 5-androstene-3,17-dione (ADI). Glutathione S-transferase A (GST-A) mRNA expression exhibited a transient, but non-significant increase following exposure to beta-NF, and generally tracked the minimal changes observed in GST-CDNB activities. Expression of the mRNA encoding glutamate-cysteine ligase catalytic subunit (GCLC), the rate-limiting enzyme in glutathione (GSH) biosynthesis, was increased 1.7-fold by beta-NF. Changes in GCLC mRNA expression were paralleled by increases in intracellular GSH. In summary, largemouth bass hepatic CYP1A-dependent and GSH biosynthetic pathways, and to a lesser extent GST, are responsive to exposure to beta-NF.

Analysis of Variance ;  Androstenedione ;  Animals ;  Bass ;  Metabolism ;  Biotransformation ;  Drug effects ;  Comparative Study ;  Cytochrome P-450 CYP1A1 ;  Biosynthesis ;  DNA Primers ;  DNA ;  Complementary ;  Genetics ;  Dinitrochlorobenzene ;  Enzyme Induction ;  Glutamate-Cysteine Ligase ;  Glutathione ;  Glutathione Transferase ;  Liver ;  Enzymology ;  Microsomes ;  Plasmids ;  Polymerase Chain Reaction ;  Methods ;  RNA ;  Messenger ;  Beta-Naphthoflavone ;  Pharmacokinetics ;  Toxicity ;