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Ethoxyresorufin‐ O ‐deethylase induction potency of polychlorinated diphenyl ethers in H4IIE rat hepatoma cells
Author(s) -
Koistinen Jaana,
Sanderson J. Thomas,
Giesy John P.,
Nevalainen Tapio,
Paasivirta Jaakko
Publication year - 1996
Publication title -
environmental toxicology and chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.1
H-Index - 171
eISSN - 1552-8618
pISSN - 0730-7268
DOI - 10.1002/etc.5620151121
Subject(s) - chemistry , aryl hydrocarbon receptor , bioassay , polychlorinated dibenzofurans , potency , aryl , environmental chemistry , enzyme inducer , cytochrome p450 , inducer , enzyme , stereochemistry , biochemistry , in vitro , organic chemistry , biology , ecology , alkyl , transcription factor , gene
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 2,3,7,8‐tetrachlorodibenzo‐ p ‐dioxin (2,3,7,8‐TCDD) 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 × 10 −5 . 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.