Bioconcentration kinetics of 2,3,7,8‐tetrachlorodibenzo‐<i>p</i>‐dioxin in rainbow trout

Branson, Dean R.; Takahashi, I. T.; Parker, William M.; Blau, Gary

doi:10.1002/etc.5620040609

Cited by 42 publications

(8 citation statements)

References 18 publications

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“…The rapid elimination of retene, in conjunction with the rapid loss of MFO activity upon transfer of trout to clean water [17], indicates that induction is transient after brief exposure because the inducer (retene) is metabolized and excreted. Hence, sustained induction will only occur during continuous exposure to retene, unlike the sustained induction caused by transient exposure to chlorinated dioxins and furans, which have much longer half—lives (8–18 weeks) [26–28].…”

Section: Discussionmentioning

confidence: 99%

Kinetics of mixed function oxygenase induction and retene excretion in retene—exposed rainbow trout (Oncorhynchus mykiss)

Fragoso

Hodson

Kozin

et al. 1999

Enviro Toxic and Chemistry

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The polycyclic aromatic hydrocarbon 7-isopropyl-1-methylphenanthrene (retene) induces mixed function oxygenase (MFO) activity of fish. Bile levels of retene and its metabolite(s) were measured in relation to exposure time, exposure concentration, and induction of MFO activity. Synchronous fluorescence spectrometry provided a rapid means of measuring the amount of retene present in the bile of exposed fish, whereas conventional fluorescence spectrometry was used to quantify the amount of retene metabolites. Based on bile analysis, increased retene exposure resulted in an increased uptake of retene and a curvilinear increase in hepatic MFO activity. Retene was present in the bile within 6 h of initial exposure. However, retene metabolite(s) only appeared in the bile after MFO induction had occurred, 12 h after exposure had commenced, suggesting that MFO activity is required for metabolism. Transfer of fish to clean water after 48 h of exposure resulted in a rapid decrease in the presence of retene and its metabolite(s) in the bile, with a calculated half-life of about 14 h. In vitro additions of retene directly to the ethoxyresorufin O-deethylase assay demonstrated that retene is capable of acting as a competitive inhibitor. Thus, retene contamination of postmitochondrial supernatant (S9 fraction) could result in false-negative results in the MFO assay. The MFO activity in extrahepatic tissues (gills, heart, and kidney) was not significantly induced with retene exposure. Thus, the major site of retene metabolism seems to be in the liver. These results confirm that retene is rapidly taken up, metabolized, and excreted by rainbow trout, and that retene metabolism and excretion are linked to hepatic MFO induction.

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Section: Discussionmentioning

confidence: 99%

Kinetics of mixed function oxygenase induction and retene excretion in retene—exposed rainbow trout (Oncorhynchus mykiss)

Fragoso

Hodson

Kozin

et al. 1999

Enviro Toxic and Chemistry

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“…Dioxin‐treated rainbow trout commonly have EROD values ranging from 100 to 1,000 pmol/min/mg [25], presumably because of the persistence of dioxins and their high affinities for the AhR. Prolonged activation of the CYP1A gene in rainbow trout, perch, and trout hepatocytes in culture is attributed to continuous binding of dioxin to the receptor complex [10,26–29]. The lower EROD values caused by retene suggest that its efficacy for activation of the AhR is lower than that of dioxin and/or that it is more readily metabolized and excreted.…”

Section: Discussionmentioning

confidence: 99%

Chronic retene exposure causes sustained induction of CYP1A activity and protein in rainbow trout (Oncorhynchus mykiss)

Fragoso

Parrott

Hahn

et al. 1998

Enviro Toxic and Chemistry

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Abstract-The removal of persistent chlorinated organic compounds from pulp mill effluents has not eliminated mixed function oxygenase (MFO) induction by these effluents. Therefore, continuous MFO induction downstream of pulp mills may be due to exposure to more labile compounds, such as retene (an alkyl-substituted phenanthrene), which typically cause transient induction after a single brief exposure. Because fish are exposed continuously to pulp mill effluents, we have tested, and rejected, the null hypothesis that continuous exposure of fish to retene does not cause sustained MFO induction. Rainbow trout exposed continuously to retene, a component of some pulp mill effluents and sediments downstream of pulp mills, showed concentration-dependent increases in hepatic ethoxyresorufin-O-deethylase (EROD) activity. The increase in EROD activity was sustained over 32 d of continuous exposure, but it diminished to background levels within 4 d after transfer to clean water. The enzymatic response was confirmed by measuring changes in the content of immunodetectable cytochrome P4501A (CYP1A) protein. These data support a role for labile, nonhalogenated compounds in chronic effects of pulp mill effluents on fish.

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“…Rainbow trout exposed to waterborne TCDD at a concentration of 320,000 pg/L exhibited a k 2 value of 0.012/ d [25], whereas carp and fathead minnows exposed to between 49 and 62 pg/L had k 2 values ranging from 0.01 to 0.013 [4]. In addition, estimates of k 2 are relatively insensitive to the high exposure concentrations used in many waterborne exposure experiments.…”

Section: Accumulation Of Tcddmentioning

confidence: 99%

ACCUMULATION OF 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN BY RAINBOW TROUT (ONCHORHYNCHUS MYKISS) AT ENVIRONMENTALLY RELEVANT DIETARY CONCENTRATIONS

Jones¹,

Kannan²,

Newsted³

et al. 2001

Environ Toxicol Chem

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Rainbow trout were fed a diet containing 1.8, 18, or 90 pg/g 3H-2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for up to 320 d. Concentrations of TCDD were determined in muscle, liver, and ovaries at 100, 150, 200, and 250 d. Concentrations of TCDD reached an apparent steady-state concentration in liver after 100 d of exposure, whereas concentrations in other tissues continued to increase until 150 d of exposure. The greatest portion of the total mass of TCDD was present in the muscle tissue with lesser proportions in other organs. As the ovaries developed before spawning, an increase occurred in the total mass of TCDD present in this tissue. The assimilation rate of TCDD during the initial 100 d of the exposure was determined to be between 10 and 30%. This is somewhat less than estimates derived based on both uptake and elimination constants determined during shorter exposures. Biomagnification factors (BMFs) were estimated for all tissues and exposure concentrations, and at all exposure periods. Lipid-normalized BMFs for muscle ranged from 0.38 to 1.51, which is consistent with the value of 1.0 predicted from fugacity theory. Uptake and depuration rate constants were determined and used to predict individual organ TCDD concentrations. Comparison with observed values indicated that the model could be used to predict tissue concentrations from the known concentrations of TCDD in food. This model will allow more refined risk assessments by predicting TCDD concentrations in sensitive tissues such as developing eggs.

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Bioconcentration kinetics of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin in rainbow trout

Cited by 42 publications

References 18 publications

Kinetics of mixed function oxygenase induction and retene excretion in retene—exposed rainbow trout (Oncorhynchus mykiss)

Kinetics of mixed function oxygenase induction and retene excretion in retene—exposed rainbow trout (Oncorhynchus mykiss)

Chronic retene exposure causes sustained induction of CYP1A activity and protein in rainbow trout (Oncorhynchus mykiss)

ACCUMULATION OF 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN BY RAINBOW TROUT (ONCHORHYNCHUS MYKISS) AT ENVIRONMENTALLY RELEVANT DIETARY CONCENTRATIONS

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