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

被引:25
作者
Koistinen, J
Sanderson, JT
Giesy, JP
机构
[1] MICHIGAN STATE UNIV, PESTICIDE RES CTR, DEPT FISHERIES & WILDLIFE, E LANSING, MI 48824 USA
[2] MICHIGAN STATE UNIV, INST ENVIRONM TOXICOL, E LANSING, MI 48824 USA
[3] UNIV JYVASKYLA, DEPT CHEM, FIN-40351 JYVASKYLA, FINLAND
关键词
polychlorinated diphenyl ethers; H4IIE bioassay; EROD; Ah receptor;
D O I
10.1002/etc.5620151121
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
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,X-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 X 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.
引用
收藏
页码:2028 / 2034
页数:7
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