Hepatic Ethoxyresorufin O-deethylase Activity Research Articles

Use of biomarkers in Nile tilapia (Oreochromis niloticus) to assess the impacts of pollution in Bolgoda Lake, an urban water body in Sri Lanka

The present study reports the first analysis of water pollutants in Sri Lankan waters using a suite of biomarkers in Nile tilapia (Oreochromis niloticus) residing in Bolgoda Lake which receives urban, industrial and domestic wastes from multiple sources. The fish were collected from the lake in the dry period (April 2005) and wet periods (September 2005, October 2006) and the levels of biomarkers viz. hepatic ethoxyresorufin O-deethylase (EROD), glutathione S-transferase (GST), metallothioneins, biliary fluorescent aromatic compounds, brain and muscle cholinesterases (ChE) were compared with those of the laboratory reared control fish and the fish obtained from a less polluted water body, Bathalagoda reservoir (reference site). The results revealed that biomarker levels of the fish collected from the reference site were not significantly different from the controls. Hepatic EROD and GST activities in fish from Bolgoda Lake were induced 4.2-16.6 folds and 1.4-3.3 folds respectively compared with the control fish. Analysis of bile in the lake fish revealed recent uptake of naphthalene, pyrene and benzo(a)pyrene type polycyclic aromatic hydrocarbons (PAHs). The induction of EROD activities in feral fish reflects the exposure of fish to aryl hydrocarbon receptor agonists including PAHs present as pollutants in the Bolgoda Lake. Cholinesterase activity in the fish inhabiting one sampling site of Bolgoda Lake was lower (22-40% inhibition) than the activity measured in the control fish indicating the presence of anticholinesterase pollutants in the area. Hepatic metallothionein levels in the lake fish were higher (1.9-3.2 folds) in comparison to the controls indicating metal exposure. The results support the potential use of these biomarkers in Nile tilapia in assessing pollution in tropical water bodies.

Piperine, a Pepper Ingredient, Improves the Hepatic Increase in Free Fatty Acids Caused by 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), are ubiquitous environmental pollutants. The variety of adverse effects produced by dioxins are a serious problem because they may affect humans and wild animals through the food chain. In this study, we examined the possible protective effects of piperine, which is a major alkaloid in black pepper (Piper nigrum Linn.) and long pepper (Piper longum Linn.), on the toxic effects of TCDD in C57BL/6J mice. The repeated administration of high doses (30 and 45 mg/kg, 14 days, p.o.) of piperine alone produced a weak agonistic effect on the aryl hydrocarbon receptor, which was evaluated based on the increase in hepatic ethoxyresorufin O-deethylase (EROD) activity. No such effect was observed at the lowest dose (15 mg piperine/kg). However, while coadministration (20 mg/kg, 28 days, p.o.) of piperine with TCDD had no effect on TCDD-induced wasting syndrome, it improved the hepatic accumulation of free fatty acids produced by TCDD. In relation to this, the hepatic accumulation of triglycerides by TCDD also tended to be reduced by piperine. Despite the above effects, piperine failed to reduce the increase in hepatic EROD activity and lipid peroxidation produced by TCDD. These results suggest that piperine is a candidate to improve disorders of lipid metabolism produced by dioxins, although the mechanism remains to be clarified.

Relation of hepatic EROD activity and cytochrome P4501A level in Sebastiscus marmoratus exposed to benzo[a]pyrene

This study was designed to investigate the in vivo effects of benzo[a]pyrene (BaP) on hepatic ethoxyresorufin- O-deethylase (EROD) activity and its correlation with cytochrome P4501A (CYP1A) protein levels in Sebastiscus marmoratus, which were exposed through a water column to BaP (10, 100, 1000 ng/L, respectively) or were treated with intraperitoneal injections of BaP (0.5, 1, 5, 10 mg/kg, respectively) every 7 d. The results showed that after 25 d of waterborne exposure to 1000 ng/L BaP, fish hepatic CYP1A levels and EROD activity were significantly induced. In contrast, EROD activity was not altered 7 d after second intraperitoneal injections, whereas, CYP1A protein levels were increased. Dose-dependent increase of biliary BaP metabolites demonstrated that the catalytic activity of CYP1A was induced by treatment with BaP. The lowest observable effect concentration with regard to biliary BaP metabolites (100 ng/L) was much lower than that with reference to EROD activity (1000 ng/L). The results suggest that biliary polycyclic aromatic hydrocarbon (PAH) metabolites were shown to better reflect the contamination gradients of PAHs than EROD activity. It appeared to be necessary to measure CYP1A protein levels to complement the EROD activity in relevant toxicological assessments.

Effects of medetomidine on hepatic EROD activity in three species of fish

Medetomidine, an antifouling candidate, was investigated for its effects on cytochrome P4501A (CYP1A) activity in fish. Rainbow trout ( Oncorhynchus mykiss), turbot ( Psetta maxima), and Atlantic cod ( Gadus morhua) were exposed to medetomidine either via i.p. injection (<5 μmol (1 mg)/kg) or via water (<50 nM). Enzyme activity was measured as ethoxyresorufin- O-deethylase (EROD) activity in liver microsomes. There was a small (2–7-fold) increase in EROD activity in rainbow trout. In turbot, EROD activity increased (4-fold) after injection, while a non-significant (50%) decrease was observed after water exposure. No effects on EROD activities were observed in Atlantic cod. In vitro inhibition studies of EROD activities in liver microsomes from all three species showed that medetomidine was a very potent CYP1A inhibitor. Thus, median inhibition values (IC 50) were 35±10 nM for rainbow trout, 47±17 nM for turbot, and 111±70 nM for Atlantic cod. These observed effects suggest that medetomidine interferes with CYP1A-dependent metabolism of xenobiotics in these fish species.

Measurement of organic contaminants and biological effects in Scottish waters between 1999 and 2005

Concentrations of organic contaminants were determined in sediment and fish collected annually at six sites around Scotland between 1999 and 2005, as part of the UK National Marine Monitoring Programme. Polycyclic aromatic hydrocarbons (PAHs) and chlorobiphenyls (CBs) were measured in sediment, while CBs and ethoxyresorufin-O-deethylase (EROD) activities were measured in the fish. Highest PAH concentrations in sediment were found at sites where higher coastal influences would be expected (e.g., Clyde and Solway) and four of the six sites gave PAH concentrations above OSPAR background assessment concentrations (BACs). A significant downward trend in the median total PAH concentrations, normalised to total organic carbon (TOC), was found at one of the six sites (Minches). The PAH profiles at all sites were consistent over the 6 year period, indicating that the sites are relatively stable and PAH sources are not changing. There was an indication of a greater petrogenic input on the west coast, with sediment from the Clyde, Solway and Minches having a greater proportion of 2- and 3-ring PAHs and a lower proportion of 5-ring PAHs. CB concentrations at all sites were low compared with UK estuarine sites and similar to sediment from more remote areas: however, BACs were exceeded. No significant trends were detected in either the sediment CB concentrations or patterns at any of the six sites. CB concentrations were significantly higher in fish liver collected from the Clyde. Concentrations at the other five sites were low, with the majority of samples having concentrations for the ICES7 CBs of <500 microg kg(-1) lipid weight. However, individual CB concentrations were still above the BACs. Hepatic EROD activities were measured in male plaice from 2002-2005 and were generally low (<10 pmol min(-1) mg protein(-1)). No temporal trends were detected in either CB concentrations or the EROD activity.

Ethoxyresorufin-O-deethylase (EROD) and vitellogenin (VTG) in flounder ( Platichthys flesus): System interaction, crosstalk and implications for monitoring

The extent to which biological systems interact in fish from multi-contaminant areas needs to be understood for full interpretation of monitoring data. This study investigates the interaction between two biomarkers, ethoxyresorufin-O-deethylase (EROD) activity and plasma vitellogenin (VTG) in the European flounder ( Platichthys flesus). Flounder were exposed to several waterborne EROD inducers and estrogenic chemicals on their own and in binary combinations. Each experimental exposure was for 10 days. The estrogenic chemicals suppressed PAH-mediated EROD induction. Ethynylestradiol (EE2) and nonylphenol (NP) had threshold concentrations of EROD inhibition similar to those at which they induced VTG production. Estradiol (E2), however, showed an ability to suppress EROD at a concentration much lower than that at which VTG was induced. This established that, although EE2 is a more potent VTG inducer than E2, it is less potent in its ability to inhibit EROD activity. The PAH, dibenz[ a, h]anthracene (DbA), showed no effect on the VTG induction caused by EE2 and E2. A small effect was noted with NP at threshold concentrations for VTG induction. Archived data on flounder hepatic EROD activity collected during estuarine monitoring were reassessed in light of the project findings. It is hypothesised that published EROD monitoring data may be an underestimation of effects if it is assumed that estrogen-mediated MFO suppression is occurring in wild populations. A greater understanding of system interaction and other factors, including genetics, that influence biomarker response to contaminants would be required to interpret biomarker monitoring data.

The Effect of Paraquat on Hepatic EROD Activity, Liver, and Gonadal Histology in Males and Females of Nile Tilapia, Oreochromis niloticus, Exposed at Different Temperatures

The activity of fish monooxygenases has been used as a monitoring tool to evaluate contamination by cytochrome P450 inducing agents. In this study ethoxyresorufin O-deethylase (EROD) activity was analyzed in males and females of Nile tilapia exposed to a low concentration of paraquat (PQ) at 17 degrees C and 27 degrees C. PQ-treated fish showed a high hepato-somatic index, except females acclimated at 17 degrees C. No differences were found for the gonado-somatic index (GSI) between males. However, PQ-treated females showed high GSI values (6.46+/-1.75) when compared with the control group (2.30+/-0.26) maintained at 27 degrees C. Males and females exposed to PQ showed higher microsomal protein values than the control group (9.46+/-0.22 vs. 6.20+/-0.18 at 17 degrees C; 9.51+/-0.35 vs. 4.70+/-0.19 mg of protein at 27 degrees C, in PQ-treated and control groups, respectively). The EROD activity was high in females exposed to PQ when compared with the control group at 17 degrees and 27 degrees C. The liver histology showed that PQ also caused some hepatic alterations of parenchyma, like vacuolization, necrosis, and an increase of macrophages aggregates and eosinophilic granular cells. Females exposed to PQ showed a greater increase of late-vitellogenic (22.2+/-3.2) and mature (12.1+/-2.0) percentage of oocytes than the control group (9.9+/-3.0 and 8.0+/-4.3, respectively), and a lower percentage of primary oocytes (8.0+/-3.3) at 27 degrees C. In short, this work has advanced new knowledge on the influence of gender in biotransformation activity and the reproductive activity of Nile tilapia exposed to a low concentration of paraquat, and demonstrated that their effects could be observed at different temperatures.

Cytochrome P4501A induction in rainbow trout gills and liver following exposure to waterborne indigo, benzo[ a]pyrene and 3,3′,4,4′,5-pentachlorobiphenyl

We have developed a gill-filament based ethoxyresorufin O-deethylase (EROD) assay to be used as a tool to monitor cytochrome P4501A (CYP1A) induction in caged fish. The present study aimed to compare temporal patterns of EROD induction in gills and liver of rainbow trout ( Oncorhynchus mykiss) exposed in the laboratory to readily metabolized and persistent CYP1A inducers, i.e. indigo, benzo[ a]pyrene (BaP), and 3,3′,4,4′,5-pentachlorobiphenyl (PCB#126). Branchial and hepatic EROD activities were examined in fish exposed for 6, 12, or 24 h and in fish exposed for 24 h and then held in clean water for 2 or 14 days. Furthermore, branchial CYP1A protein expression was localized by immunohistochemistry. All compounds strongly induced branchial EROD activity within 6 h. The highest EROD inductions observed for indigo, BaP, and PCB#126 were roughly similar in gills (52-, 76-, and 74-fold), but differed considerably in liver (11-, 78-, and 200-fold). In indigo- and BaP-exposed fish, both hepatic and branchial EROD activities decreased rapidly in clean water. In PCB#126-exposed fish, decreased branchial and increased hepatic EROD activities were observed following transfer to clean water. The substances gave rise to immunostaining for CYP1A at different cellular sites. All inducers increased the CYP1A-immunostaining in the gill filament secondary lamellae, but PCB#126 also induced a pronounced CYP1A immunoreactivity in cells near the basal membrane of the epithelium of the primary lamellae. The observation that the low BaP and indigo concentrations induced EROD activity markedly in the gills but only slightly or not at all in the liver, supports the contention that readily metabolized AhR agonists may escape detection when hepatic EROD activity is used for environmental monitoring. The results show that gill filament EROD activity is a sensitive biomarker both for persistent and readily metabolized AhR agonists in polluted water.

Ethoxyresorufin- O-deethylase (EROD) activity and bile metabolites as contamination indicators in Baltic Sea perch: Determination by HPLC

Exposure of Baltic Sea perch ( Perca fluviatilis) to organic contaminants was investigated by means of liver enzyme activity, measured as ethoxyresorufin- O-deethylase (EROD) activity, and PAH metabolites excreted to bile. Female perch used in the study were caught in coastal waters of the western Gulf of Finland. Reaction conditions were optimised for determination of EROD activity in liver. A high-performance liquid chromatography (HPLC) method with fluorescence detection was developed to separate the interfering fluorescent signal from the signal due to EROD activity. EROD activity in perch varied within a concentration range of 0.30–14 pmol min −1 mg −1 protein. Recent PAH exposure was indicated in enhanced levels of the bile metabolite 1-hydroxypyrene, which varied between 213 and 1149 μg kg −1. No correlation was indicated between hepatic EROD activity and concentration of 1-hydroxypyrene.

Enhancement of Dioxin Toxicity with an Anti-Stress Drug, Carbenoxolone, in Mice

The effect of the carbenoxolone (CBX) on the subacute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied in C57BL/6J mice. The loss of body weight due to TCDD was enhanced by simultaneous treatment with CBX. In agreement with the change in body weight, CBX failed to improve TCDD-induced hepatic hypertrophy and thymic atrophy. Co-treatment of CBX with TCDD tended to cause hepatic hypertrophy more extensively than did TCDD alone, and combined treatment induced significant renal hypertrophy and splenic atrophy which were not seen in mice treated with TCDD or CBX alone. CBX had no effect on the TCDD-mediated induction of hepatic ethoxyresorufin O-deethylase activity, a marker for aryl hydrocarbon receptor (AhR)-linked gene expression. These results suggest that CBX enhances TCDD toxicity by a mechanism(s) distinct from activation of the AhR.

Low hepatic ethoxyresorufin‐o‐deethylase activity correlates with high organochlorine concentrations in Atlantic tomcod from the Canadian east coast

A suppression of hepatic ethoxyresorufin-O-deethylase (EROD) activity was reported recently in large-sized Atlantic tomcod (Microgadus tomcod) from the St. Lawrence Estuary (SLE; QC, Canada), possibly related to chronic exposure to persistent contaminants and/or to emaciation. In the present study, hepatic concentrations of organochlorine contaminants and biological responses were measured in female tomcods from three estuaries located on the Canadian east coast: The SLE, the Miramichi (ME), and the Richibucto (RE) Rivers Estuaries (NB, Canada). Tomcods from the SLE had higher hepatic concentrations of organochlorine contaminants than tomcods from the ME and RE. For example, concentrations of polychlorinated biphenyls (PCBs, lipid wt) were 2.5 to 4 times higher, and concentrations of mirex and chlordanes were 6 times higher, in tomcods from the SLE than in tomcods from the other sites. Concentrations of polycyclic aromatic hydrocarbons (PAHs) metabolites in the bile did not differ among sites. The pattern of biological responses differed markedly between the SLE and the two other sites. Tomcods from the SLE had 1.5 times higher concentrations of DNA adducts and 2 times higher rates of hepatocellular proliferation, but 20 times lower hepatic EROD activity, than tomcods from the ME and RE. Lipid content was not correlated with EROD activity, indicating that low hepatic lipid content alone does not cause suppression of EROD activity in Atlantic tomcod. In contrast, for the three sites combined, EROD activity decreased as concentrations of PCBs increased. Within sites, hepatic PCB concentrations increased as lipid content decreased. This study supports the hypothesis that low EROD activity in SLE tomcods is related to chronic exposure to organochlorine contaminants.

Cytological changes in association with ethoxyresorufin O‐deethylase induction in fish upon dietary exposure to benzo[a]pyrene

Juvenile areolated grouper (Epinephelus areolatus) were exposed to two levels of dietary benzo[a]pyrene (BaP; 0.25-12.5 microg/g body wt/d) for four weeks, followed by four weeks of depuration. Significant increase in hepatic ethoxyresorufin O-deethylase (EROD) activities was found after one week, preceding an increase in lipopigments (as measured by quantitative transmission electron microscopy) in week 2 of exposure. The EROD activities in the BaP-treated fish subsided at week 4 of exposure and throughout the depuration period. Lipopigments in the high-dose group appeared to be more persistent than that of the EROD activity during the exposure period and remained significantly higher than that of the controls at week 4. Levels of lipopigments, however, rapidly subsided on withdrawal of BaP exposure. These results appear to suggest that changes in EROD activities would precede cytological changes and that both the observed cytological and biochemical changes are reversible. Results of the present study also lend further support to our earlier findings on Solea ovata, that a significant relationship exists between EROD activity and lipopigment accumulation (as measured by volume density, absolute volume, numerical density, and absolute density; r = 0.483-0.358, p < 0.05), regardless of fish species (S. ovata and aerolated grouper) as well as the routes of exposure to BaP (intraperitoneal injection or dietary exposure). This provides strong supporting evidence that elevated EROD activities in fish liver do not merely indicate exposure to polyaromatic hydrocarbons (PAHs) but are also associated with significant biological effects. Our results showed that hepatic EROD activity and lipopigments could be used to indicate recent exposure of the fish to BaP/PAHs.

Reduction of the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice using an antiulcer drug, geranylgeranylacetone.

The protective effect of geranylgeranylacetone (GGA), an antiulcer drug, against the acute toxicity and teratogenicity produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was examined in C57BL/6J mice. When mice were co-treated, GGA reduced the loss of body weight gain and lethality produced by TCDD but hepatomegaly and thymic atrophy were not improved. Additionally, no protective effect of GGA was observed in the formation of cleft palate and hydronephrosis in mouse fetuses caused by maternal exposure to TCDD. To clarify the reducing mechanism by GGA, the Hsp70.1 mRNA levels in liver and intestine were analyzed. However, it was difficult to explain the effect of GGA from the induction of Hsp70.1. GGA had also no effect on the induction of hepatic ethoxyresorufin O-deethylase activity by TCDD. These data suggest that GGA exhibits a protective effect against some forms of dioxin toxicity by a mechanism without involving inhibition of arylhydrocarbon receptor activation.

Curcumin Anticipates the Suppressed Body Weight Gain with 2,3,7,8-Tetrachlorodibenzo-p-Dioxin in Mice

The protective effect of curcumin, a potent inducer of heat shock protein (Hsp) 70, against the acute toxicity produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was studied in vivo in C57BL/6J mice. Curcumin reduced the loss of body weight gain produced by TCDD regardless of having no effect on hepatomegaly and thymic atrophy. Hsp70.1 mRNA levels in liver and intestine were unaffected or tended to be reduced by TCDD and/or curcumin treatment. Curcumin also had no effect on the induction of hepatic ethoxyresorufin O-deethylase activity by TCDD. These data suggest that curcumin exhibits a protective effect against some forms of dioxin toxicity by a mechanism(s) distinct from the increase in hepatic and intestinal Hsp70 and inhibition of arylhydrocarbon receptor activation.

Hepatic CYP1A levels and EROD activity in English sole: biomonitoring of marine contaminants in Vancouver Harbour.

To assess chemical contaminant stress in the marine environment, ethoxyresorufin-O-deethylase (EROD) activity and cytochrome P450 1A (CYP1A) expression were measured in 88 English Sole (Pleuronectes vetulus) collected during May and June 1999 from four sites in Vancouver Harbour and at an expected reference site outside the harbour. Hepatic microsomes were prepared from the fish and analyzed for total CYP content, EROD activity, and CYP1A protein levels. Hepatic EROD activity and CYP1A protein levels were elevated in fish from two sites in the inner harbour. A comparison with sediment chemistry data showed that fish with increased EROD activity and CYP1A levels came from sites containing relatively high levels of polycyclic aromatic hydrocarbons and polychlorinated biphenyls. Unexpectedly high levels of EROD activity and CYP1A protein were also found in fish from a reference site near Gibsons, in Howe Sound. The elevated EROD activity and CYP1A expression in fish from this site cannot be explained by the chemical analysis data collected.

Evaluation of biomarkers of exposure and effect in juvenile areolated grouper (Epinephelus areolatus) on foodborne exposure to benzo[a]pyrene

Food-borne benzo[a]pyrene (B[a]P) was administered daily to juvenile grouper (Epinephelus areolatus) at two environmentally realistic concentrations (a low dose of 0.25 microg B[a]P/g body wt/d and a high dose of 12.5 microg B[a]P/g body wt/d) to investigate and relate temporal changes in body burden of B[a]P, hepatic ethoxyresorufin-O-deethylase (EROD) activities, growth, RNA:DNA ratio, estradiol, testosterone, and triiodothyronine (T3). After feeding with B[a]P diets for four weeks, fish were fed with normal diet for another four weeks to study recovery of the various biomarkers during the depuration period. After one week of exposure, both body muscle B[a]P burdens and hepatic EROD activities significantly increased. Body burdens were stable in tissues until the fourth week of exposure, when concentrations in the high-dose group increased markedly, at which time a concomitant decrease in EROD was found. During the depuration period, body burdens decreased in the second week, and EROD declined in the first week. Growth and RNA:DNA ratio were unaltered. Despite large variations found in sex steroid levels, elevation of testosterone was clearly evident in the fourth week, showing that B[a]P may disrupt the balance of sex steroids in fish. Significantly, increases in plasma-free T3 concentrations were found in the fourth week of exposure and the first week of depuration, suggesting that development and reproduction may potentially be at risk during chronic exposures. Our data also suggest that these hormonal disturbances are not persistent and that normal hormonal levels can be restored soon after contamination is abated.

Ecotoxicological Risks Associated with Land Treatment of Petrochemical Wastes. II. Effects on Hepatic Phase I and Phase II Detoxification Enzymes in Cotton Rats

The purpose of this study was to evaluate possible exposure and resultant hepatic effects of petrochemical waste on cotton rats (Sigmodon hispidus) living on landfarmed sites. Male and female cotton rats were collected in summer, fall, and winter from four landfarm sites and four ecologically similar reference sites. Hepatic methoxyresorufin O-deethylase (MROD) activity was significantly induced in male and female rats collected from landfarms compared to rats collected from reference sites. In contrast, changes in ethoxyresorufin O-deethylase (EROD) activity were inconsistent due to season, sex, and treatment variation. A significant decrease in EROD and MROD activity was found in cotton rats held for 48 h prior to sacrifice compared to rats euthanized on the day of capture. These results indicate that when using hepatic EROD and MROD activities as biochemical markers of exposure to aryl hydrocarbon receptor agonists, animals should be euthanized as quickly as possible after capture. The cotton rats collected from one landfarm unit exhibited a pattern of consistent elevation of EROD, MROD, and pentoxyresorufin O-deethylase (PROD) activity. This unit also had a pattern of elevated CYP1A2 protein expression determined by Western blotting. There were no consistent alterations from contaminant exposure on hepatic glutathione S-transferase (GST) activity, glutathione levels, or CYP1A1 protein. Hepatic EROD and MROD activities varied considerably between seasons and sex of rats. In conclusion, consistent induction of hepatic EROD and MROD activities in cotton rats was found in three out of four sampled landfarm sites compared to the rats collected from the reference sites, indicating exposure to contaminants--likely polyaromatic hydrocarbons.

Hepatic EROD activity is not a useful biomarker of polychlorinated biphenyl exposure in the adult herring gull (Larus argentatus).

Liver concentrations of polychlorinated biphenyls (PCBs) and chicken embryo hepatocyte (CEH) bioassay-derived 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents (TCDD-EQs) were measured in livers of adult herring gulls (Larus argentatus) collected from several locations on the Great Lakes and two reference sites. Total PCB concentrations (sum of 42 congeners) and TCDD-EQ concentrations were compared with hepatic ethoxyresorufin-O-deethylase (EROD) activity, methoxyresorufin-O-deethylase (MROD) activity and immunodetectable cytochrome P4501A (CYP1A) protein concentration. EROD and MROD activity were not significantly correlated with total PCB concentration or TCDD-EQ concentration in liver tissue. CYP1A protein concentration was significantly correlated with total PCB concentration, but the linear relationship had little predictive power. We conclude that EROD is not a useful biomarker of PCB exposure in the adult herring gull.

Endocrine effects of sublethal exposure to persistent organic pollutants (POPs) on silver carp ( Hypophthalmichthys molitrix)

Silver carp ( Hypophthalmichthys molitrix) samples were collected from five selected sites that represent diverse levels of downgraded persistent organic pollutants (POPs) contamination in Ya-Er Lake in October 1999. Hepatic ethoxyresorufin-O-deethylase (EROD) and UDP glucuronosyltransferase (UDPGT) activities, hepatosomatic index (HSI), hepatic retinoids, serum thyroid hormones were measured. It was found that hepatic retinol and serum free 3,5,3′- tetraiodothyronine (FT 3) significantly increased ( P<0.01) when both hepatic EROD and UDPGT activities significantly declined ( P<0.01) from pond 1 to 5 with decrease in the degree of pollution. This significant negative correlation ( P<0.01) suggests that the persistent organochlorinated contaminants could induce hepatic EROD and UDPGT activities, alter retinoid and thyroid hormone homeostasis, and finally lead to the reduction of retinol and FT 3, the two biologically active forms of retinoids and thyroid hormone in silver carp of Ya-Er Lake.

Vitamin and thyroid status in arctic grayling ( Thymallus arcticus) exposed to doses of 3,3 ′,4,4 ′-tetrachlorobiphenyl that induce the phase I enzyme system

Induction of phase I biotransformation enzymes is recognized as a hallmark response in fish exposed to coplanar PCBs. Depletions of vitamins A and E and disrupted thyroid hormone and glandular structure secondary to this induction have not yet been examined in an arctic fish species. Arctic grayling were exposed to a single oral dose of 0 (control), 10, 100 or 1000 ng 3,3 ′,4,4 ′-tetrachlorobiphenyl (TCB) g −1 bodyweight, a contaminant found in most arctic fish. After 30 and 90 days of exposure, TCB concentrations in tissues, hepatic phase I activity (as ethoxyresorufin-O-deethylase (EROD)), plasma and tissue vitamin A and E concentrations, plasma thyroid hormone levels and thyroid glandular structure were examined. Total plasma osmolality, as an indicator of overall fish health was also monitored. TCB recovery in tissues was low and extremely variable, making comparisons between intended dose groups inappropriate. Therefore, correlation analysis between actual recovered TCB concentrations and biochemical responses was employed. Hepatic EROD activity correlated strongly with liver TCB concentrations. Liver concentrations of vitamin A were altered as a function of TCB concentrations and EROD activity, but plasma vitamin A status was not affected. Vitamin E was depleted by TCB accumulation in blood and EROD induction in liver of males only at 90 days post-exposure. Thyroid hormones status and glandular structure were not affected by the short duration TCB exposures used in this experiment. TCB concentrations were correlated with an elevation in plasma osmolality. Results from this experiment indicate that the vitamin status and osmoregulation of arctic grayling exposed to TCB can be compromised. Further studies of field populations exposed to this type of contaminant are warranted.