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Ethoxyresorufin O-deethylase (EROD) and aryl hydrocarbon hydroxylase (AHH)-inducing potency and lethality of chlorinated naphthalenes in chicken (Gallus domesticus) and eider duck (Somateria mollissima) embryos
Section of Environmental Toxicology, Uppsala University, Uppsala, Sweden.ORCID iD: 0000-0001-7338-2079
Section of Environmental Toxicology, Uppsala University, Uppsala, Sweden.
Environmental Chemistry, Wallenberg Laboratory, Stockholm University, Stockholm, Sweden.
1994 (English)In: Archives of Toxicology, ISSN 0340-5761, E-ISSN 1432-0738, Vol. 68, no 1, 37-42 p.Article in journal (Refereed) Published
Abstract [en]

The 7-ethoxyresorufin O-deethylase (EROD)- and aryl hydrocarbon hydroxylase (AHH)-inducing potencies and lethalities of a technical preparation of polychlorinated naphthalenes (PCNs) (Halowax 1014, approx imate congener ratio: 20% tetrachloronaphthalenes, 40% pentachloronaphthalenes, 40% hexachloronaphthalenes), a mixture of 50% 1,2,3,5,6,7-hexachloronaphthalene and 50% 1,2,3,4,6,7-hexachloronaphthalene (HxCN-mix), and 1,2,3,4,5,6,7-heptachloronaphthalene (HpCN) were studied in chicken (Gallus domesticus) and elder duck (Somateria mollissima) embryos. Mortality and hepatic EROD activity were determined on day 10 of incubation in chicken embryos exposed to various doses of the PCNs via the air-sacs of the eggs on day 7. The HxCN-mix and Halowax 1014 proved to have both embryolethal and EROD-inducing properties, while the HpCN had low EROD-inducing potency and embryolethality. ED(50) values for EROD induction by the HxCN-mix and Halowax 1014 were estimated to be 0.06 mg/kg egg and 0.2 mg/kg egg, respectively. Fifty percent of the chicken embryos died (6/12) when given 3.0 mg/kg of the HxCN-mix while a similar dose of Halowax 1014 caused mortality in 4 out of 12 chicken embryos. The dose-response curve for EROD induction by Halowax 1014 exhibited a decline after the maximal level was reached. When Halowax 1014 (1.0 mg/kg, egg) was coinjected with 3,3',4,4',5-pentachlorobiphenyl (PCB IUPAC #126) (0.1 mu g/kg egg) no additive effects on EROD activity were found, but when the same dose of Halowax 1014 was coinjected with a dose of PCB #126, known to cause maximal induction (1.0 mu g/kg egg), the resulting EROD activity was lower than that caused solely by 1.0 mu g PCB #126/kg egg. These findings indicate that Halowax 1014 has both EROD-inducing and EROD-inhibiting properties. Mortality and EROD and AHH activities were determined on day 18 (chicken) or day 24 (elder) of incubation in embryos exposed to 1.0 mg/kg egg via the yolk-sac on day 4 (chicken) or day 5 (elder). The HxCN-mix and Halowax 1014 induced AHH and EROD in both chicken and elder, but the induction rates were higher in the elder embryos. The HxCN-mix and Halowax 1014 caused degenerative hepatic lesions and pericardial oedema in the chicken embryos but not in the elder embryos. The most toxic PCNs tested (the HxCN-mix and Halowax 1014) were approximately of the same EROD-inducing potency as previously found for the most toxic mono-ortho-chlorinated biphenyls (Brunstrom 1990), and 1000 times less toxic and potent as EROD inducers compared with PCB #126 (Brunstrom and Andersson 1988). HpCN was considerably less toxic and exhibited a low EROD-inducing potency. The chicken embryos were more sensitive to the hepatotoxic effects produced by Halowax 1014 and the HxCN-mix than the elder duck embryos, while the elder embryos were more responsive in terms of EROD and AHH induction. The two HxCNs studied usually make up approximately 1% of the total quantity of PCNs present in Halowax 1014 [when determined with gas chromatography (flame ionization detection)]. Therefore, the relatively high toxic potency of Halowax 1014 cannot be explained by its content of the two HxCNs.

Place, publisher, year, edition, pages
1994. Vol. 68, no 1, 37-42 p.
Keyword [en]
chick embryos; eider embryos; environmental pollutants; enzyme induction; polychlorinated naphthalenes; toxicity
National Category
Environmental Sciences
Research subject
Enviromental Science
Identifiers
URN: urn:nbn:se:oru:diva-41351DOI: 10.1007/s002040050030ISI: A1994MU86500006PubMedID: 8166603Scopus ID: 2-s2.0-0028157951OAI: oai:DiVA.org:oru-41351DiVA: diva2:780372
Available from: 2015-01-14 Created: 2015-01-14 Last updated: 2016-12-02Bibliographically approved

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