Accumulation, depuration and hepatic mixed-function oxidase enzyme induction in juvenile rainbow trout and lake whitefish exposed to dietary 2,3,7,8-tetrachlorodibenzo -p-dioxin

Fisk, Aaron T.; Yarechewski, Alvin L.; Metner, D.A.; Evans, R. E.; Lockhart, W.L.; Muir, Derek C.G.

doi:10.1016/s0166-445x(96)00817-x

Cited by 28 publications

(29 citation statements)

References 40 publications

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“…Our results were consistent with the TCDD bioaccumulation model of Fisk and colleagues (1997) of TCDD bioaccumulation at the 100 ppb dose range at 42 d despite a relatively limit of detection in our study. Using Fisk's model as a guide, we expected quantifiable TCDD concentrations show dose-dependent accumulation in fish, and this was confirmed with the second analytical measurement.…”

Section: Discussion and Summarysupporting

confidence: 91%

“…The trout in our study were younger and smaller than those reported in the study of Fisk and colleagues (1997), which necessitated the use of multiple fish per extraction; the young age and low body fat of fish in the current study were likely responsible for the low overall TCDD concentrations detected. This suggested deviation from the model in younger and smaller rainbow trout at the lower dosage range.…”

Section: Discussion and Summarycontrasting

confidence: 55%

“…Based on previous reports recorded in the Pesticide Action Network (PAN) Pesticide Database (http://www.pesticideinfo.org/), most dietary TCCD exposures have been performed in juvenile fish larger than 3 g or in adults. Previous research reported that juvenile rainbow trout (3-7 g) did not exhibit an increase in relative lethality after dietary TCDD at 494 ppt in food over 13 weeks (Kleeman et al, 1986), and dietary TCDD at 413 ppt in food caused 13% mortality in larger juvenile trout (5-9 g) after 180 d (Fisk et al, 1997; Hektoen et al, 1994). In juvenile rainbow trout with 35 g of body weight, LD50 of TCDD ranges from 7 to 15 ppb (Spitsbergen et al, 1988b).…”

Section: Discussion and Summarymentioning

confidence: 99%

“…We compared accumulation of dietary TCDD in whole rainbow trout to the model developed by Fisk et al (1997).…”

Section: Methodsmentioning

confidence: 99%

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Gene expression and pathologic alterations in juvenile rainbow trout due to chronic dietary TCDD exposure

et al. 2013

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The goal of this project was to use functional genomic methods to identify molecular biomarkers as indicators of the impact of TCDD exposure in rainbow trout. Specifically, we investigated the effects of chronic dietary TCDD exposure on whole juvenile rainbow trout global gene expression associated with histopathological analysis. Juvenile rainbow trout were fed Biodiet starter with TCDD added at 0, 0.1, 1, 10 and 100 ppb (ng TCDD / g food), and fish were sampled from each group at 7, 14, 28 and 42 days (d) after initiation of feeding. 100 ppb TCDD caused 100% mortality at 39 d. Fish fed with 100 ppb TCDD food had TCDD accumulation of 47.37 ppb (ng TCDD / g fish) in whole fish at 28 d. Histological analysis from TCDD-treated trout sampled from 28 d and 42 d revealed that obvious lesions were found in skin, oropharynx, liver, gas bladder, intestine, pancreas, nose and kidney. In addition, TCDD caused anemia in peripheral blood, decreases in abdominal fat, increases of remodeling of fin rays, edema in pericardium and retrobulbar hemorrhage in the 100 ppb TCDD-treated rainbow trout compared to the control group at 28 d. Dose- and time-dependent global gene expression analyses were performed using the cGRASP 16,000 (16K) cDNA microarray. TCDD-responsive whole body transcripts identified in the microarray experiments have putative functions involved in various biological processes including growth, cell proliferation, metabolic process, and immune system processes. Nine microarray-identified genes were selected for QPCR validation. CYP1A3 and CYP1A1 were common up-regulated genes and HBB1 was a common down-regulated gene among each group based on microarray data, and their QPCR validations are consistent with microarray data for the 10 and 100 ppb TCDD treatment groups after 28-d exposure (p< 0.05). In addition, in the 100 ppb group at 28d, expression of complement component C3-1 and trypsin-1 precursor have a more than 10-fold induction from the microarray experiments, and their QPCR validations are consistent and showed significant induction in the 100 ppb group at 28d (p< 0.05). Overall, lesion in nasal epithelium is a novel and significant result in this study, and TCDD-responsive rainbow trout transcripts identified in the present study may lead to the development of new molecular biomarkers for assessing the potential impacts of environmental TCDD on rainbow trout populations.

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Section: Discussion and Summarysupporting

confidence: 91%

Section: Discussion and Summarycontrasting

confidence: 55%

Section: Discussion and Summarymentioning

confidence: 99%

“…We compared accumulation of dietary TCDD in whole rainbow trout to the model developed by Fisk et al (1997).…”

Section: Methodsmentioning

confidence: 99%

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Gene expression and pathologic alterations in juvenile rainbow trout due to chronic dietary TCDD exposure

et al. 2013

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“…Whitefish seems little more sensitive than rainbow trout (Fisk et al 1997) and effects in the Baltic Sea strains are thus unlikely. Elevated rates of mortality and deformations in Baltic cod have been found but contaminants seem an unlikely cause in comparison to other factors; also the peak recruitment during peak exposures (in late 1970's) is evidence against their role (Vallin et al 1999).…”

Section: Fishmentioning

confidence: 99%

Risks and Management of Dioxins and Dioxin-like Compounds in Baltic Sea Fish: An Integrated Assessment

2006

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Dietary accumulation and depuration of hydrophobic organochlorines: Bioaccumulation parameters and their relationship with the octanol/water partition coefficient

Fisk

Norstrom

Cymbalisty

et al. 1998

Enviro Toxic and Chemistry

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329

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Dietary accumulation of 23 hydrophobic organochlorines (OCs) by juvenile rainbow trout (Oncorhynchus mykiss) was studied with the objective of obtaining relationships between bioaccumulation parameters and the octanol/water partition coefficient (Kow). A wide range of OCs were used including 16 polychlorinated biphenyls (PCBs 18, 28, 44, 52, 66, 101, 105, 118, 128, 138, 153, 187, 189, 195, 206, and 209), hexachlorobenzene, mirex, tris(4‐chlorophenyl)methane (TCPMe), tris(4‐chlorophenyl)methanol (TCPMeOH), and three toxaphene congeners (Cl7‐chlorobornane [CHB] [Hp‐sed], Cl8‐CHB [T2], and Cl9‐CHB [T12]). Tris(4‐chlorophenyl)methane (half‐life [t1/2] = 65 d) was more persistent than TCPMeOH (t1/2 = 20 d), and TCPMe was not biotransformed to TCPMeOH by rainbow trout. Cl7‐chlorobornane (t1/2 = 32 d) was more rapidly eliminated, and appears to be more readily metabolized, than Cl8‐CHB (t1/2 = 43 d) and Cl9‐CHB (t1/2 = 42 d). With the exception of TCPMeOH, Cl7‐CHB, and PCB 18, all of the OCs had biomagnification factors (BMFs) >1, implying a potential to biomagnify. Half‐lives had a significant curvilinear relationship with Kow (R2 = 0.85, p < 0.001), with a maximum t1/2 for OCs with log Kow ∼ 7.0. Decreasing t1/2 for OCs of log Kow > 7.0 may be related to slow kinetics of these super hydrophobic OCs and the short exposure phase, which results in insufficient time for the super hydrophobic OCs to reach slower clearing compartments of the rainbow trout. Assimilation efficiency was not as well described by Kow as by t1/2 and BMF, although a significant curvilinear relationship was observed (R2 = 0.53, p = 0.004). The BMF had a significant curvilinear relationship with log Kow (R2 = 0.84, p < 0.001). Recalcitrant OCs with a log Kow of ∼7.0 would appear to have the greatest potential for food chain biomagnification in fish.

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Accumulation, depuration and hepatic mixed-function oxidase enzyme induction in juvenile rainbow trout and lake whitefish exposed to dietary 2,3,7,8-tetrachlorodibenzo -p-dioxin

Cited by 28 publications

References 40 publications

Gene expression and pathologic alterations in juvenile rainbow trout due to chronic dietary TCDD exposure

Gene expression and pathologic alterations in juvenile rainbow trout due to chronic dietary TCDD exposure

Risks and Management of Dioxins and Dioxin-like Compounds in Baltic Sea Fish: An Integrated Assessment

Dietary accumulation and depuration of hydrophobic organochlorines: Bioaccumulation parameters and their relationship with the octanol/water partition coefficient

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