RAINBOW-TROUT HEPATIC MIXED-FUNCTION OXYGENASE INDUCTION BY POLYCHLORINATED DIBENZO-P-DIOXINS (PCDDS) AS A FUNCTION OF TIME AND TISSUE CONCENTRATION

Rainbow trout, dosed orally with 0.060-84 mu g/kg of [H-3]-2,3,7,8-tet rachlorodibenzo-p-dioxin (TCDD), [C-14]-1,2,3,4,7,8-hexachlorodibenzo- p-dioxin (HxCDD), or [C-14]- 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD) showed dose-dependent increases in hepatic ethoxyresorufin O- deethylase (EROD) activity, up to 250-fold, after 2-16 d. Induction of EROD activity was a sensitive and rapid indicator of exposure to PCDD s. The effects of time after exposure were not dramatic, but generally EROD activity after 2 d was lower than EROD activity after 16 d. Slop es of dose-response curves relating EROD activity to hepatic concentra tions of PCDDs significantly decreased and intercepts significantly in creased with increasing Lime of exposure. When fish were grouped by or al doses, only the low doses of TCDD and HpCDD exhibited time-dependen t EROD induction, with significantly greater activity 16 d after dosin g compared to 2 d. In most cases, hepatic and muscle concentrations of PCDDs did not significantly change over rime. Concentrations of PCDDs in liver and muscle accounted for up to 7% of the orally administered dose. Hepatic levels of PCDDs ranged from 20-100 pg/g at the lowest d oses to about 1000 pg TCDD/g, 2000 pg HxCDD/g, or 40,000 pg HpCDD/g al the highest doses. Of the PCDD in the liver, approximately one-third to one-half was associated with the postmitochondrial supernatant (PMS ). PCDD concentrations in muscle did not span as wide a range of conce ntrations as did PCDD in liver; fish given low doses had 10 pg/g in mu scle whereas fish given high doses had several hundred picograms per g ram in muscle for all three PCDDs.