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. 2012 Mar 5;109(12):4479–4484. doi: 10.1073/pnas.1118467109

Table 1.

CYP1A activity of HaCaT cells exposed to inhibitors of CYP1A in commercial DMEM (Com) or in DMEM prepared with purified tryptophan (Pure)

% inhibition
Induction
Compound (concentration) Com Com Pure
TCDD (1 nM) 24.1 ± 1.48ns 24.5 ± 2.03
Trioxalen (1 μM) 33.0 ± 9.1* 1.48 ± 0.18** 0.05 ± 0.03
Ketoconazole (10 μM) 69.7 ± 1.7*** 1.31 ± 0.22*** 0.27 ± 0.05
Ellipticine (0.05 μM) 43.3 ± 3.4*** 9.01 ± 1.03*** 3.88 ± 0.32
Genistein (10 μM) 14.2 ± 5.3ns 1.10 ± 0.07*** 0.02 ± 0.04
Diosmin (10 μM) 40.8 ± 3.3** 0.79 ± 0.06*** 0.18 ± 0.04
α-Naphtoflavone (0.25 μM) 62.2 ± 2.9*** 1.46 ± 0.14*** 0.08 ± 0.03
Cycloheximide (18 μM) 65.8 ± 1.9*** 3.45 ± 0.33*** 0.27 ± 0.04
α-Tocopherol (50 μM) 14.9 ± 6.2ns 0.54 ± 0.03*** 0.13 ± 0.02
DMSO (0.1%, vol/vol) 0.25 ± 0.04*** 0.05 ± 0.02
EtOH (0.1%, vol/vol) 0.33 ± 0.04** 0.16 ± 0.03

Percent inhibition of TCDD-induced EROD activity following 6 h of exposure in the absence of any other addition; means ± SE of triplicate measurements. Significance of inhibition compared with TCDD is depicted with asterisks (ns, non significant; *P < 0.05; **P < 0.01; ***P < 0.001).

Mean EROD activity (pmol resorufin/mg protein) ± SE following 12 h of exposure. Differences in EROD induction for respective treatment in the commercial compared with the pure media were tested. ns, non significant; *P < 0.05; **P < 0.01; ***P < 0.001. EROD induction at several time points is shown in Fig. S6.