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P O Darnerud - One of the best experts on this subject based on the ideXlab platform.

  • induction of 7 Ethoxyresorufin o deethylase erod activity in mice foetuses by the pcb congener 3 3 4 4 tetrachlorobiphenyl
    Xenobiotica, 1993
    Co-Authors: T Sinjari, U Tornwall, P O Darnerud
    Abstract:

    1. 3,3′,4,4′-Tetrachlorobiphenyl (TCB) induces liver microsomal 7-Ethoxyresorufin-O-deethylase (EROD) activity, and this P450 isoform, i.e. CYP 1, is involved in the metabolism of TCB.2. TCB administered i.p. to pregnant mice (5-25mg/kg) induced foetal as well as maternal hepatic EROD activity; in all cases the maternal induced activity was higher than the foetal activity. EROD activity of TCB-induced foetuses increased with developmental age, but decreased with the length of time after treatment.3. Strain differences were seen; in control mice and TCB-treated dams NMRI>C57BL in EROD activity, but in transplacentally TCB-treated foetuses, C57BL>NMRI. EROD activity in non-pregnant control C57BL mice was higher than in pregnant ones, whereas no activity was seen in control foetuses.4. Results indicate that TCB at a certain dose can induce foetal metabolism, but that earlier observed foetal accumulation at lower TCB doses is probably a consequence of transplacental transport of maternally-produced metabolites.

  • Induction of 7-Ethoxyresorufin-O-deethylase (EROD) activity in mice foetuses by the PCB-congener 3,3′,4,4′-tetrachlorobiphenyl
    Xenobiotica, 1993
    Co-Authors: T Sinjari, U Tornwall, P O Darnerud
    Abstract:

    1. 3,3′,4,4′-Tetrachlorobiphenyl (TCB) induces liver microsomal 7-Ethoxyresorufin-O-deethylase (EROD) activity, and this P450 isoform, i.e. CYP 1, is involved in the metabolism of TCB.2. TCB administered i.p. to pregnant mice (5-25mg/kg) induced foetal as well as maternal hepatic EROD activity; in all cases the maternal induced activity was higher than the foetal activity. EROD activity of TCB-induced foetuses increased with developmental age, but decreased with the length of time after treatment.3. Strain differences were seen; in control mice and TCB-treated dams NMRI>C57BL in EROD activity, but in transplacentally TCB-treated foetuses, C57BL>NMRI. EROD activity in non-pregnant control C57BL mice was higher than in pregnant ones, whereas no activity was seen in control foetuses.4. Results indicate that TCB at a certain dose can induce foetal metabolism, but that earlier observed foetal accumulation at lower TCB doses is probably a consequence of transplacental transport of maternally-produced metabolites.

Martin Van Den Berg - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of Ethoxyresorufin o deethylase erod activity in mixtures of 2 3 7 8 tetrachlorodibenzo p dioxin and polychlorinated biphenyls erod acitivity as biomarker in tcdd and pcb risk assessment
    Environmental Science and Pollution Research, 1995
    Co-Authors: Mats Tysklind, A T C Bosveld, Patrik L Andersson, Eeske Y Verhallen, Theo L Sinnige, Willem Scinen, Christoffer Rappe, Martin Van Den Berg
    Abstract:

    Induction of Ethoxyresorufin-O-deethylase (EROD) activity and porphyrin accumulation shows different structure-activity relationships for different polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Interactions between the two responses can strongly influence the induction and activity of EROD. The results support the conclusion that there are nonadditive interactions between nondioxin-like PCBs and dioxin-like compounds. The interaction between EROD activity and the porphyrin biosynthesis makes the prerequisite of additivity in the toxic equivalency factor concept for environmental mixtures highly spurious. Inhibition of EROD activity caused by non-dioxin like compounds could have a significant impact on the value of EROD activity as a biomarker in the present methods of risk assessment for these compounds.

  • Absence of interactions on hepatic retention and 7-Ethoxyresorufin-O-deethylation activity after co-administration of 1,2,3,7,8-pentachlorodibenzo-p-dioxin and 2,4,5,2′,4′,5′-hexachlorobiphenyl
    Toxicology, 1992
    Co-Authors: Joost De Jongh, Fred Wondergem, Willem Seinen, Martin Van Den Berg
    Abstract:

    Abstract Interactions between 1,2,3,7,8-pentachlorodibenzo- p -dioxin (PnCDD) and 2,4,5,2′,4′,5′-hexachloro-biphenyl (HxCB) on hepatic retention of PnCDD and on cytochrome P450 related enzyme activities were studied in male C57BL/6J mice. Animals received 8 nmol PnCDD/kg orally, alone or in combination with 1–416 μmol HxCB/kg. Co-administration of HxCB did not alter the hepatic retention of PnCDD or the 7-Ethoxyresorufin- O -deethylation (EROD) activity induced by PnCDD as observed after 1 week. A small antagonistic effect on total cytochrome P450 content and 7-Ethoxyresorufin- O -deethylation (PROD) activity was observed at a dose of 8 nmol PnCDD/kg and 1 μmol HxCB/kg. Furthermore, a significant induction of PROD activity by PnCDD was found. This was not expected, since PROD activity is considered to be a specific marker for CYP2b related enzyme activity and this type of cytochrome P450 is not induced by polychlorinated dibenzo- p -dioxins such as PnCDD. It is concluded that, under these short-term experimental conditions, no toxicokinetic basis was found to explain the antagonistic effects on hepatic cytochrome P450 related activities observed in the present study or in other studies.

Helmut Segner - One of the best experts on this subject based on the ideXlab platform.

  • fixed effect level toxicity equivalents a suitable parameter for assessing Ethoxyresorufin o deethylase induction potency in complex environmental samples
    Environmental Toxicology and Chemistry, 2000
    Co-Authors: Werner Brack, Helmut Segner, Monika Moder, Gerrit Schuurmann
    Abstract:

    Within the scope of bioassay-directed identification of dioxin-like toxicants in complex environmental samples, EC50-based and fixed-effect-level-based 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity equivalents (TEQs) were compared to assess 7-Ethoxyresorufin-O-deethylase (EROD) inducing potency of sediment fractions using the rainbow trout liver cell line RTL-W1 as bioassay system. Toxicity equivalents on the basis of fixed effect levels are suggested in order to minimize interpretation problems due to the superposition of enzyme-inducing and enzyme-inhibiting effects. Bioassay-directed fractionation of a contaminated sediment extract in the industrial region of Bitterfeld (Germany) based on fixed-effect-level TEQs indicated high dioxin-like activity in the lipophilic sediment fractions containing the prototypic arylhydrocarbon receptor (AhR) agonists polychlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAHs). However, only a small part of the EROD induction could be attributed to the PCBs and PAHs that were analyzed. Significant EROD induction occurred also with some of the more polar fractions.

  • Fixed-effect-level toxicity equivalents—a suitable parameter for assessing Ethoxyresorufin-O-deethylase induction potency in complex environmental samples
    Environmental Toxicology and Chemistry, 2000
    Co-Authors: Werner Brack, Helmut Segner, Monika Moder, Gerrit Schuurmann
    Abstract:

    Within the scope of bioassay-directed identification of dioxin-like toxicants in complex environmental samples, EC50-based and fixed-effect-level-based 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity equivalents (TEQs) were compared to assess 7-Ethoxyresorufin-O-deethylase (EROD) inducing potency of sediment fractions using the rainbow trout liver cell line RTL-W1 as bioassay system. Toxicity equivalents on the basis of fixed effect levels are suggested in order to minimize interpretation problems due to the superposition of enzyme-inducing and enzyme-inhibiting effects. Bioassay-directed fractionation of a contaminated sediment extract in the industrial region of Bitterfeld (Germany) based on fixed-effect-level TEQs indicated high dioxin-like activity in the lipophilic sediment fractions containing the prototypic arylhydrocarbon receptor (AhR) agonists polychlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAHs). However, only a small part of the EROD induction could be attributed to the PCBs and PAHs that were analyzed. Significant EROD induction occurred also with some of the more polar fractions.

  • transient induction of 7 Ethoxyresorufin o deethylase erod activity by medium change in the rainbow trout liver cell line rtl w1
    Marine Environmental Research, 2000
    Co-Authors: Helmut Segner, Anja Behrens, Kristin Schirmer, E M Joyce, Niels C Bols
    Abstract:

    Cytochrome P4501A (CYP1A) metabolizes a wide array of lipophilic xenobiotics. In fish liver, CYP1A is constitutively expressed at low levels, but xenobiotics can strongly induce CYP1A expression via a receptor-mediated pathway. While induction of hepatic CYP1A in teleosts by xenobiotics is well investigated, very little is known on the regulation of constitutive CYP1A expression and its induction by factors other than xenobiotics. In the present study we show that in the rainbow trout liver cell line, RTL-W1, CYP1A-catalyzed 7-Ethoxyresorufin-O-deethylase (EROD) activity can be induced by a change of the culture medium, in the absence of xenobiotics. The increase in cellular EROD levels is of transient nature. Experiments with cell incubation solutions supplemented with various medium components indicate that photooxidized tryptophan is the agent causing the increase of EROD activity after medium change.

  • microassay for rapid measurement of 7 Ethoxyresorufin o deethylase activity in intact fish hepatocytes
    Marine Environmental Research, 1998
    Co-Authors: Anja Behrens, Kristin Schirmer, Niels C Bols, Helmut Segner
    Abstract:

    Abstract In vitro assays using isolated fish cells are increasingly used to measure the induction of cytochrome P4501A (CYP1A) and its associated enzyme activity, 7-Ethoxyresorufin-O-deethylase (EROD). Compared to permanent cell lines, primary hepatocyte cultures represent an in vitro system that is closer to the in vivo situation, and, therefore, may be a particularly suitable model to study physiological and xenobiotic regulation of CYP1A expression. The application of conventional EROD assays to primary hepatocyte cultures, however, suffers from some disadvantages such as the labour-intensity and the need for high cell numbers per sample. In this report, we present an approach for assessment of EROD activity in teleost hepatocytes cultured in 48-well plates without the need for preparation of microsomes. The assay is based on the method of (Kennedy, S. W., Lorenzen, A., James, C. A. and Collins, B. T. (1993) Anal. Biochem. 211, 102–112.) but employs live instead of dead cells. For EROD detection, 7-Ethoxyresorufin is added directly to the live cells and its metabolism to resorufin is observed by repeated measurements over 20 min in a fluorescence plate reader. The assay does not require the addition of exogenous NADPH. Resorufin utilization through cytoplasmic DT-diaphorase has to be inhibited by addition of dicoumarol. Disturbance by conjugate formation accounts to not more than 20% of total resorufin formed. After measurement, the cells can be washed and, after continued incubation, can be used for further assays.

Biyan Wang - One of the best experts on this subject based on the ideXlab platform.

  • screening toxicological effects of different contaminants using hepatic homogenates based Ethoxyresorufin o deethylase in vitro
    Science of The Total Environment, 2020
    Co-Authors: Biyan Wang, Hai Yan Wang
    Abstract:

    In this paper, we demonstrated the potential of an in vitro method of liver homogenate-based Ethoxyresorufin-O-deethylase (EROD) to determine the toxicological effects of multiple kinds of contaminants. We evaluated the in vitro impact of nine pharmaceutically active compounds (PhACs), 13 polycyclic aromatic hydrocarbons (PAHs), and three polychlorinated biphenyls (PCBs). There were different responses of EROD to these contaminants. The response of EROD to PhACs was quite complex, exhibiting both induction and inhibition effects. PAHs and PCBs elicited a strong inhibitory response on EROD activity at high concentrations in a dose-dependent manner. PAHs showed more inhibitory effects as the number of benzene rings increased. Our in vitro bioassay seems to be a potential method for toxicological screening of multiple types of contaminants.

  • in vitro effects of brominated flame retardants selected metals and their mixtures on Ethoxyresorufin o deethylase activity in mossambica tilapia liver
    Ecotoxicology and Environmental Safety, 2018
    Co-Authors: Hai Yan Wang, Biyan Wang, Dan Xiao
    Abstract:

    Abstract The in vitro effects of individual brominated flame retardants (BFRs), selected metals, and their binary mixtures on Ethoxyresorufin-O-deethylase (EROD) activity were evaluated using a plate-reader method. The BFRs, 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47), decabromodiphenyl oxide (BDE-209), hexabromocyclododecane (HBCD), and tetrabromobisphenol A (TBBPA), were tested at doses ranging from 0.1 ng/L to 100 µg/L. Selected metals (Cu2+, Cd2+, Hg2+, and Zn2+) were screened at doses of 0.1 mg/L to 50 mg/L. The activity of EROD was significantly induced by TBBPA, BDE-209, and Zn2+, while HBCD, Cu2+, Cd2+, and Hg2+ decreased EROD activity. Moreover, following exposure to binary mixtures of metals and BFRs, the EROD activity dose-response curves were similar to those of the metals alone, indicating that EROD activity was governed by the metals.

Eckhard Loser - One of the best experts on this subject based on the ideXlab platform.

  • comparative studies on the induction of Ethoxyresorufin o deethylase by 2 3 7 8 tcdd and 2 3 7 8 tbrdd
    Chemosphere, 1990
    Co-Authors: Tetsuji Nagao, Diether Neubert, Eckhard Loser
    Abstract:

    Ethoxyresorufin O-deethylase (EROD) activity was measured in rat liver homogenates subsequent to a single subcutaneous injection of 2,3,7,8-tetrabromodibenzo-p-dioxin (TBrDD). The rate of induction was compared with that observed after treatment with the corresponding chlorinated substance (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD) using the same experimental set-up. The time-dependence of the induction profile of EROD activity after treatment with 600 ng TBrDD/kg body wt was almost identical with that observed after an injection of 300 ng TCDD/kg body wt. When measured 7 days after the injection the extent of EROD induction was largely linear (in a double logarithmic plot) over the concentration range between 0.02 to 6 nmole TBrDD/kg body wt. The results of our studies indicate that TBrDD is a similarly powerful inducer of EROD in rat liver as TCDD.