Effects of chlorinated diphenyl ethers on the mixed-function oxidases and ultrastructure of rat and trout liver*1

Chui, Y. C.; Hansell, M.M.; Addison, R.F.; Law, F. C. P.

doi:10.1016/0041-008x(85)90165-6

Cited by 34 publications

(8 citation statements)

References 20 publications

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“…The mechanisms of toxicity and the toxic potency of PCDEs to fish and other vertebrates is not clear at present. Chlorinated diphenyl ethers do not appear to induce hepatic monoxygenases in teleosts [20]. Several PCDEs were reported as immunosuppressive in mice, and the immunotoxic potency of these compounds appeared to be correlated with monoxygenase‐inducing potency [18,19].…”

Section: Resultsmentioning

confidence: 99%

“…PCDEs have been shown to suppress the immune response in mice, and the immunotoxic potency of individual PCDE compounds was positively correlated with aryl hydrocarbon hydroxylase (AHH) induction potency [18,19]. Chui et al [20] reported that 2,4,4′‐triCDE and 2,4,4′,5‐tetraCDE both induced elevated AHH activity in rat liver, but these compounds did not elevate AHH significantly above controls in rainbow trout liver.…”

Section: Introductionmentioning

confidence: 99%

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Early life‐stage mortalities of Japanese medaka (Oryzias latipes) exposed to polychlorinated diphenyl ethers

Metcalfe

Cormier

et al. 1997

Enviro Toxic and Chemistry

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Abstract-Polychlorinated diphenyl ethers (PCDEs) are a group of compounds that resemble polychlorinated dibenzofurans in structure that have been detected at ppb concentrations in fish from the Great Lakes. The objective of this project was to determine the toxicological significance of PCDE residues in fish. PCDE congener 77 (3,3Ј,4,4Ј-tetrachlorodiphenyl ether), congener 71 (2,3Ј,4Ј,6-tetrachlorodiphenyl ether), congener 118 (2,3Ј,4,4Ј,5-pentachlorodiphenyl ether), and congener 105 (2,3,3Ј,4,4Ј-pentachlorodiphenyl) were tested for toxicity with early life stages (ELS) of Japanese medaka, Oryzias latipes. These embryotoxicity data showed that the mono-ortho congeners 105 and 118 and the non-ortho congener 77 were embryotoxic to medaka. However, the toxic equivalency factors (TEFs) estimated for congeners 105, 77, and 118 relative to 2,3,7, 8-TCDD were relatively low at 0.00056, 0.00003, and 0.00001, respectively. PCDE compounds were isolated in a fraction prepared from a bulk extract of Lake Ontario lake trout.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Early life‐stage mortalities of Japanese medaka (Oryzias latipes) exposed to polychlorinated diphenyl ethers

Metcalfe

Cormier

et al. 1997

Enviro Toxic and Chemistry

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“…Polychlorinated diphenyl ethers have been reported to induce hepatic monooxygenases in fish and rodents [23,24,[26][27][28] and …”

Section: Introductionmentioning

confidence: 99%

Ethoxyresorufin‐O‐deethylase induction potency of polychlorinated diphenyl ethers in H4IIE rat hepatoma cells

Koistinen

Sanderson

Giesy

et al. 1996

Enviro Toxic and Chemistry

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Abstract-Polychlorinated diphenyl ethers (PCDEs) are structurally similar to polychlorinated biphenyls (PCBs), and some PCDE congeners have been reported to cause toxic responses similar to those caused by some of the non-ortho-substituted PCBs, which are mediated by the aryl hydrocarbon receptor (AhR). Twenty-nine PCDEs were tested for their potency as AhR agonists relative to 2,3,7,3,7, by measuring their ability to induce the cytochrome P-450 1A1-associated enzyme activity, ethoxyresorufin-O-deethylase (EROD), in the H4IIE rat hepatoma cell bioassay. All PCDE congeners tested were found to be inactive as EROD inducers except for PCDE 156, which was a weak EROD inducer with a 2,3,7,8-TCDD equivalency factor of about 1.2 ϫ 10 Ϫ5 . During this study we determined that small amounts of polychlorinated dibenzofurans (PCDFs) that occurred as impurities in the PCDE preparations were the cause of the apparent EROD induction initially measured in our experiments. Once the PCDF impurities were removed by purification on florisil, little or no activity could be attributed to the PCDEs.

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“…The outcome of this study is in agreement with structural considerations suggesting that the nonplanarity of halogenated DEs results in a low binding affinity to the Ah receptor (93). Nevertheless, some studies have shown that pure PCDEs indeed are weak inducers of microsomal EROD and AHH activities in a congener-and conformation-specific manner (94)(95)(96)(97).…”

Section: Experimental Animalsmentioning

confidence: 99%

Polybrominated diphenyl ethers: occurrence, dietary exposure, and toxicology.

Darnerud

Eriksen

Johannesson

et al. 2001

Environ Health Perspect

686

263

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Polybrominated diphenyl ethers (PBDEs) are used as flame retardants in plastics (concentration, 5--30%) and in textile coatings. Commercial products consist predominantly of penta-, octa-, and decabromodiphenyl ether mixtures, and global PBDE production is about 40,000 tons per year. PBDEs are bioaccumulated and biomagnified in the environment, and comparatively high levels are often found in aquatic biotopes from different parts of the world. During the mid-1970--1980s there was a substantial increase in the PBDE levels with time in both sediments and aquatic biota, whereas the latest Swedish data (pike and guillemot egg) may indicate that levels are at steady state or are decreasing. However, exponentially increasing PBDE levels have been observed in mother's milk during 1972--1997. Based on levels in food from 1999, the dietary intake of PBDE in Sweden has been estimated to be 0.05 microg per day. Characteristic end points of animal toxicity are hepatotoxicity, embryotoxicity, and thyroid effects as well as maternal toxicity during gestation. Recently, behavioral effects have been observed in mice on administration of PBDEs during a critical period after birth. Based on the critical effects reported in available studies, we consider the lowest-observed-adverse-effect level (LOAEL) value of the PBDE group to be 1 mg/kg/day (primarily based on effects of pentaBDEs). In conclusion, with the scientific knowledge of today and based on Nordic intake data, the possible consumer health risk from PBDEs appears limited, as a factor of over 10(6) separates the estimated present mean dietary intake from the suggested LOAEL value. However, the presence of many and important data gaps, including those in carcinogenicity, reproduction, and developmental toxicity, as well as additional routes of exposure, make this conclusion only preliminary. Moreover, the time trend of PBDEs in human breast milk is alarming for the future.

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Effects of chlorinated diphenyl ethers on the mixed-function oxidases and ultrastructure of rat and trout liver*1

Cited by 34 publications

References 20 publications

Early life‐stage mortalities of Japanese medaka (Oryzias latipes) exposed to polychlorinated diphenyl ethers

Early life‐stage mortalities of Japanese medaka (Oryzias latipes) exposed to polychlorinated diphenyl ethers

Ethoxyresorufin‐O‐deethylase induction potency of polychlorinated diphenyl ethers in H4IIE rat hepatoma cells

Polybrominated diphenyl ethers: occurrence, dietary exposure, and toxicology.

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