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1 M) and cytochrome P450 (SKF525A, 100 microM; ethoxyresorufin, 10 microM; metyrapone, 500 microM; pipe
2 ere compared with the commercial substrate 7-ethoxyresorufin (7-ER).
3 aiaretic acid (a lipoxygenase inhibitor) nor ethoxyresorufin (a cytochrome P450 inhibitor) altered th
4 e used to determine kcat and Km values for 7-ethoxyresorufin and phenacetin O-deethylation and the (i
5 n secretion, urea synthesis, deethylation of ethoxyresorufin (CYT P450 activity), and responsiveness
6  substantial inhibition of CYP1A2-mediated 7-ethoxyresorufin de-ethylation in the presence of HO-1, w
7 creening for 1A2 activity (deethylation of 7-ethoxyresorufin) identified two functional P450 hybrids
8        Reconstituted CYP1A1-Val462 catalyzed ethoxyresorufin metabolism at a slightly but significant
9 mance liquid chromatography determination of ethoxyresorufin metabolism) of cytochrome P-450 (CYP) 1A
10  environmental contaminants on cytotoxicity, ethoxyresorufin O-deethylase (EROD) activity, and mRNA e
11 453), as analyzed by both immunoblotting and ethoxyresorufin O-deethylase activity.
12 e, total CYP1A1 activity, as measured by the ethoxyresorufin O-deethylase assay, was detected in mito
13 the four model reaction activities, that is, ethoxyresorufin O-deethylation (CYP1A1/2), between five
14 ituted with NADPH-P450 reductase, rates of 7-ethoxyresorufin O-deethylation and phenacetin O-deethyla
15 B1 enzymatic activity was evaluated using an ethoxyresorufin O-deethylation assay in transfected HEK-
16  vitro inactivation of scup CYP1A activity 7-ethoxyresorufin O-deethylation by TCB was time dependent
17 ryonic hepatocytes to determine effects on 7-ethoxyresorufin-O-deethylase (EROD) activity and mRNA ex
18 (TK) locus, CYP1A activity was determined by ethoxyresorufin-O-deethylase (EROD) activity and qRT-PCR
19 HF-FPWs resulted in significant induction of ethoxyresorufin-O-deethylase (EROD) activity in both liv
20 5000 mug/L fluoxetine resulted in elevated 7-ethoxyresorufin-O-deethylase (EROD) activity of cytochro
21 romatic hydrocarbons (PAHs) for induction of ethoxyresorufin-O-deethylase (EROD) activity was assesse
22 ryonic hepatocytes to determine effects on 7-ethoxyresorufin-O-deethylase (EROD) activity, porphyrin
23 morant hepatocytes to determine effects on 7-ethoxyresorufin-O-deethylase (EROD) activity, porphyrin
24 species by determining (i) the activities of ethoxyresorufin-O-deethylase (EROD) and glutathione-S-tr
25 hpf); CYP1 activity was determined by in ovo ethoxyresorufin-o-deethylase (EROD) at 96 hpf, and cardi
26 essary for the induction of CYP1A1-dependent ethoxyresorufin-o-deethylase (EROD) enzymatic activity b
27 h several cytochrome P450 isoforms (CYPs): 7-ethoxyresorufin-O-deethylase (EROD), benzyloxy-4-[triflu
28   Moreover, corresponding enzyme activities (ethoxyresorufin-O-deethylase (EROD), CAT, SOD, and GR) w
29                              CYP1A1-mediated ethoxyresorufin-O-deethylase activity and amounts of its
30 he tested compounds induced CYP1A-associated ethoxyresorufin-O-deethylase activity in mouse embryos o
31 thyronine (T3), hepatic biotransformation (7-ethoxyresorufin-O-deethylase activity), or oxidative str
32 0 (CYP) 1A1 and 1B1 activity, as measured by ethoxyresorufin-O-deethylase activity, in cells treated
33 2 and 20 hours after shock, as determined by ethoxyresorufin-O-deethylase activity, metabolism of BaP
34 ent inhibitor of cytochrome P4501A1-mediated ethoxyresorufin-O-deethylase activity, with an IC50 of 0
35 A1 protein by Western blotting and exhibited ethoxyresorufin-O-deethylase activity; neither the CHO-n
36 xperimental results for in vitro and in vivo ethoxyresorufin-O-deethylase and vitellogenin induction
37                                           An ethoxyresorufin-O-deethylase assay was performed on thes
38  7-ethoxyresorufin showed a stimulation of 7-ethoxyresorufin-O-deethylation in the mixed reconstitute
39 eriments using the 1A2-preferred substrate 7-ethoxyresorufin showed a stimulation of 7-ethoxyresorufi