Induction effects of polychlorinated biphenyls,polycyclic aromatic hydrocarbons and other widespread aromatic environmental pollutants on microsomal monooxygenase activities in chick embryo liver |
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Authors: | M Machala Lenka Mátlová Ivan Svoboda Karel Nezveda |
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Institution: | (1) Veterinary Research Institute, 62132 Brno, Czech Republic, XX;(2) Masaryk University, Faculty of Science, 60237 Brno, Czech Republic, XX |
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Abstract: | Cytochrome P450-dependent 7-ethoxyresorufin O-deethylase (EROD), 7-pentoxyresorufin O-dealkylase (PROD) and 7-ethoxycoumarin O-deethylase (ECOD) activities in 14-day-old chick embryo livers were determined 24 h after pretreatment with selected widespread
aromatic environmental contaminants, including polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs),
hexachlorobenzene, and dialkylesters of phthalic acid, and compared with the inducing potencies of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the coplanar and mono-o-chlorinated PCBs. The effects of other model inducers, i.e. phenobarbital and pyrazole, were also examined. Specificity of
EROD induction was estimated with regard to contaminants frequently present in environmental samples and dose-response curves
for EROD induction were determined. A strong induction (comparable with that by mono-o-chlorinated biphenyl treatment) by dibenzoa,h]anthracene, benzok]fluoranthene or benzob]fluoranthene was found, but the
maximal level of EROD activity inducible by TCDD was not achieved, partly due to the high toxicity of the tested PAHs. 3-Methylcholanthrene
showed moderate inducing potencies; benza]anthracene, benzoa]pyrene, chrysene and 2,2′,3,4,4′,5′-hexachlorobiphenyl appeared
to be weak inducers. Other PAHs and PCBs tested, as well as hexachlorobenzene, dialkyl phthalates, phenobarbital and pyrazole
had no marked effects on the EROD level. ECOD activities were increased non-specifically by TCDD, 3-methylcholanthrene, hexachlorobenzene
and phenobarbital. A significant enhancement of PROD activity by TCDD and related inducers was observed, while phenobarbital
induced the PROD activity only weakly; SDS-PAGE analysis showed that the chicken phenobarbital-inducible cytochromes P4502H
with apparent molecular weights 50 kDa were not markedly induced by the TCDD- or 3-methylcholanthrene treatments. Inhibition
of EROD and PROD by 9-hydroxyellipticine, a specific inhibitor of rat hepatic cytochrome P4501A1, revealed that PROD induction
by TCDD and other P4501A-inducers was probably a result of a broader substrate specificity of chick embryo P4501A. Measurement
of EROD activities in chick embryo liver is highly sensitive, specific and suitable for the determination of TCDD-type toxicity
of new drugs, agrochemicals, and industrial pollutants.
Received: 4 January 1995 / Accepted: 28 September 1995 |
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Keywords: | Chick embryo Cytochrome P450 Environmental pollutants Polychlorinated biphenyls Polycyclic aromatic hydrocarbons 2 3 7 8-Tetrachlorodibenzo-p-dioxin Phenobarbital |
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