Sanderson · Toxicological sciences : an official journal of the Society of Toxicology 2001 · in vitro comparative study · n=?

2,3,7,8-Tetrachlorodibenzo-p-dioxin and diindolylmethanes differentially induce cytochrome P450 1A1, 1B1, and 19 in H295R human adrenocortical carcinoma cells.

Cited 64 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

In vitro cell culture study (bench research with no human clinical data)

PubMed 11294972 · doi:10.1093/toxsci/61.1.40 · record verified 2026-08-29

What was done

H295R human adrenocortical carcinoma cells were exposed for 24 hours to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 0–30 nM), diindolylmethane (DIM, 0–10 µM), or structural DIM analogs. Ethoxyresorufin-O-deethylase (EROD) activity was measured as an index of CYP1A1 and CYP1B1 activity, aromatase (CYP19) activity was measured by conversion of 1 beta-(3)H-androstenedione to estrone and (3)H2O, and mRNA expression was analyzed for CYP1A1, CYP1B1, and CYP19.

What was found

TCDD and DIM induced EROD activity with EC50 values of approximately 0.3 nM and 3 µM, respectively. DIM, but not TCDD, induced aromatase activity with an apparently maximal 2-fold increase at 10 µM (higher concentrations were cytotoxic). TCDD at 30 nM significantly increased CYP1A1 and CYP1B1 mRNA levels without affecting CYP19 mRNA. DIM at 3 µM significantly increased mRNA levels for CYP1A1, CYP1B1, and CYP19. Analogs with substitutions at the 5 and 5' positions (3 µM) induced aromatase and EROD activity and mRNA for all three CYPs, whereas central carbon-substituted analogs showed little or no inductive activity.

Why it matters

This study shows that DIM and specific 5,5'-substituted analogs can upregulate aromatase (CYP19) expression and activity in adrenocortical cells, differentiating them from pure Ah receptor agonists like TCDD that do not induce aromatase.

Limits

The findings are limited to an in vitro model using a single human adrenocortical carcinoma cell line (H295R), which cannot replicate systemic pharmacokinetics, tissue distribution, or in vivo hormonal interactions. Sample sizes and statistical variability metrics were not reported in the abstract.

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