Abstract

1. 1. Rainbow trout hepatic microsomes were pre-incubated in vitro with 1 pM, 1 nM, and 1 μM acrylamide for 20 or 30 min and ethoxyresorufin- O-deethylase (EROD) was measured. In vitro preincubation did not produce a significant decrease in EROD catalytic activity. 2. 2. The effects of 50 ppm acrylamide monomer on hepatic CYP1A1 mRNA and CYP1A1 isozyme steady state levels in rainbow trout were determined after 6, 10, and 14 days of exposure. 3. 3. Acrylamide monomer produced a 35% increase, 51% decrease and 140% increase in CYP1A1 mRNA at 6, 10 and 14 days, respectively, while at the same time CYP1A1 isozyme levels were decreased 12%, 67%, and 62% and EROD activity was decreased 33%, 90%, and 86%, respectively. 4. 4. This indicates that acrylamide treatment may result in either a change in the translation of CYP1A1 mRNA or an isozyme selective inactivation of CYP1A1 resulting in loss of CYP1A1 apoprotein. 5. 5. The effect of acrylamide treatment on hepatic CYP1A1 induction was determined using 10 or 14 day treatment with 50 ppm aerylamide monomer in a flowthrough exposure and induction with betanaphthoflavone (β-NF; 100 mg/kg i.p.) for 1 or 4 days. 6. 6. Acrylamide and 1-day β-NF had no effect on CYP1A1 mRNA levels when compared to 1-day β-NF treatment alone, but acrylamide and 4-day β-NF resulted in a 74% decrease in CYP1A1 mRNA compared to 4-day β-NF treatment alone. 7. 7. This indicates that while the initial induction response (1-day) to β-NF is not affected by acrylamide treatment, the full induction response over 4 days was inhibited by acrylamide due to decreased CYP1A1 mRNA levels, possibly by effects of acrylamide and/or a metabolite(s) on the transcription of CYP1A1 mRNA or by decreasing the stability of CYP1A1 mRNA.

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